Forensic Toxicology A Comparative Approach, 2e [Second Edition] 9789390158478

Table of contents :
Cover
Half Title Page
Title Page
Copyright
Dedication
Preface to the Second Edition
Acknowledgments
Preface to the First Edition
Acknowledgments
Competencies
Contents
1. General Toxicology
2. Preservation of Viscera and Other Materials
3. Forensic Science Laboratory and Analytical Methods Including Psychoanalysis
4. Corrosives
5. Mechanical Irritants
6. Non-Metallic Inorganic Chemical Irritants
7. Irritants: Inorganic Metallic Poison
8. Agricultural Poison: Pesticides
9. Plant and Vegetable Irritants
10. Animal Irritants
11. Somniferous Poison: Opium and its Alkaloids
12. Inebriant Poison: Alcohols
13. Deliriant Poisons: Datura, Cannabis and Cocaine
14. Cerebral Depressant
15. Cerebral Stimulant
16. Hallucinogens
17. Spinal Poisons
18. Peripheral Nerve Poisons
19. Cardiac Poisons
20. Asphyxiant and Irrespirable Poisons
21. Drug Dependence and Abuse
22. Food Poisoning
23. War Gases: Chemical and Biological
Appendix
Multiple Choice Questions
Index
Back Cover

Citation preview

Second Edition

Forensic Toxicology A Comparative Approach As per the latest

CBME Guidelines | Competency Based Undergraduate Curriculum for the Indian Medical Graduate • For MBBS, Postgraduate Students of Forensic Medicine and Toxicology, and BPMT Students • For Students Preparing for NEET-PG and other Entrance Examinations • Reference Guide for Clinicians and Medical Officers Dealing in Forensic-Toxicological Emergencies

Second Edition

Forensic Toxicology A Comparative Approach As per the latest

CBME Guidelines | Competency Based Undergraduate Curriculum for the Indian Medical Graduate • For MBBS, Postgraduate Students of Forensic Medicine and Toxicology, and BPMT Students • For Students Preparing for NEET-PG and other Entrance Examinations • Reference Guide for Clinicians and Medical Officers Dealing in Forensic-Toxicological Emergencies

Vipul Ambade

MBBS, MD, LLB

Professor and Head Department of Forensic Medicine Government Medical College Gondia, Maharashtra

CBS Publishers & Distributors Pvt Ltd New Delhi • Bengaluru • Chennai • Kochi • Kolkata • Lucknow • Mumbai Hyderabad

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Disclaimer Science and technology are constantly changing fields. New research and experience broaden the scope of information and knowledge. The authors have tried their best in giving information available to them while preparing the material for this book. Although, all efforts have been made to ensure optimum accuracy of the material, yet it is quite possible some errors might have been left uncorrected. The publisher, the printer and the authors will not be held responsible for any inadvertent errors, omissions or inaccuracies. eISBN: xxxx Copyright © Authors and Publisher Second eBook Edition: 2022 All rights reserved. No part of this eBook may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, recording, or any information storage and retrieval system without permission, in writing, from the authors and the publisher. Published by Satish Kumar Jain and produced by Varun Jain for CBS Publishers & Distributors Pvt. Ltd. Corporate Office: 204 FIE, Industrial Area, Patparganj, New Delhi-110092 Ph: +91-11-49344934; Fax: +91-11-49344935; Website: www.cbspd.com; www.eduport-global.com; E-mail: [email protected]; [email protected] Head Office: CBS PLAZA, 4819/XI Prahlad Street, 24 Ansari Road, Daryaganj, New Delhi-110002, India. Ph: +91-11-23289259, 23266861, 23266867; Fax: 011-23243014; Website: www.cbspd.com; E-mail: [email protected]; [email protected].

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Representatives Hyderabad Pune Nagpur Manipal Vijayawada Patna

to my parents Late Shri Namdeorao Ambade and Smt Chandraprabha Ambade

Preface to the Second Edition I

am deeply overwhelmed after completing the compilation of the material of the second edition of the book Forensic Toxicology: A Comparative Approach. Since publishing the first edition, students, readers, and faculty forum have shared their views, comments and suggestions, particularly regarding the references. When I started to work on the second edition I thought it would be a breeze to add modification, recent advances and references, compared to the Herculean task of creating and publishing the first edition. However, once the work commenced, I realized that this revision would require even greater effort than the first edition; and the prevailing COVID-19 pandemic added further hurdles in it. The most obvious change in the second edition is the inclusion of the references in the running literature in superscript and at the end of each chapter. The treatment pertaining to poisoning is often overlooked in forensic texts and not considered in clinical practice. Management of poisoning has been upgraded to the latest trends to be useful in clinical practice for the physician. The bedside/color test for the detection of different types of poisoning has been greatly updated. Specific Learning Objectives (SLOs) for each chapter as per the competency based learning recommended by the Medical Council of India for medical graduates have been incorporated. Important questions and MCQs are included in this edition to help students prepare for theory as well as practical examinations.

Vipul Ambade [email protected]

Acknowledgments S

ince the release of the first edition in 37th Annual Conference of Indian Academy of Forensic Medicine held at BJ Medical College, Ahmedabad, Gujarat, on 17th January, 2016, many students, readers and faculty forums have shared their views, comments and suggestions. To all of them, including in particular the following, my deepest sincere thanks: Dr Chetan Jani, Dr Kalidas Chavan, Dr Numan Hussaini, Dr Rajesh Bardale, Dr Harshwardhan Khartade, Dr Ravindra Deokar, Dr Ulhas Gonnade, Dr Shailendra Dhawne, Dr Jaideo Borkar, Dr Ajit Malani, Dr Manish Tiwari, Dr Ajay Taware, Dr Amol Shinde, Dr Naresh Zanzad, Dr SK Singhal, Dr Ajit Pathak, Dr Mohan Pawar, Dr Pawan Sable, Dr Swapnil Akhade, Dr Pawan Tekade, Dr Sharad Kuchewar, Dr Sachin Gadge, Dr Ravi Meshram, Dr Arun Jaiswani, Dr Ashok Najan, Dr Dayanand Kolpe, Dr Amol Maiyyar, Dr Arti Narde, Dr Shailesh Wakde, Dr Ajay Shendarkar, Dr Praveen Jadhav, Dr Pratik Gilbe, Dr Indrajeet Khandekar and many more with special thanks to Dr Manu Sharma for his overall technical support during the correction of revised edition of this book. I would also like to acknowledge the unquestionable support of CBS Publishers & Distributors and Mr YN Arjuna (Senior Vice President—Publishing, Editorial and Publicity) along with his entire team for excellent formatting of this book. Lastly, I am thankful to my wife Dr Hemlata, lovely daughters Vidhi and Aarohi, and my relatives and friends for helping me accomplish the task and extend their support even during the prevailing COVID-19 pandemic.

Vipul Ambade

Preface to the First Edition I

t is a great pleasure that I am presenting the book Forensic Toxicology: A Comparative Approach. Taking into consideration that toxicology is very vast and difficult to remember, this book is presented in a simple and lucid language. The most important distinguishing feature of this book is that the different poisons of a group are discussed in a comparative point-wise manner in a tabular form for better understanding, learning and easy comparison. Apart from the numerous tabular charts, more than 180 photographs and figures related to poison/autopsy findings are included in this book. A separate chapter on preservation of viscera and other materials containing guidelines for collection, preservation and dispatch; and a new chapter on biological and chemical warfare are also included. Latest trends in the management of poisoning cases have been tried to cover in the book. While preparing this book, I have gone through various textbooks and journals, and I am indebted to these authors. This book is primarily designed for undergraduate students and I hope it will make toxicology easier for students to learn and study. It will surely help the postgraduate students in preparing for examination and prove useful to the medical officers/ practitioners while dealing the case of poisoning. I would definitely welcome the valuable suggestion and healthy criticism, which will be of immense help for future improvement of this book.

Vipul Ambade [email protected]

Acknowledgments I

began my career in forensic medicine about 20 years back under the guidance of my teacher Dr AC Mohanty, a man with great vision and tremendous knowledge. While working with him, he not only made me realize the importance of the subject but also changed my outlook towards the dead victim. I gratefully acknowledge him for his guidance and influence which made me to persist my career in forensic. It is with a great pleasure and deep sense of gratitude that I acknowledge my debt to my respected teacher Dr AP Dongre (Ex-Dean, Government Medical College, Yeotmal) for his affectionate guidance and constant support. I am indebted to my revered teacher Dr AN Keoliya (Dean, Government Medical College, Gondia) for fostering me while learning and exploring my potential for different administrative and non-administrative work. I am obliged to Dr Abhimanyu Niswade (Dean, Government Medical College, Nagpur) for allowing to embrace this work in the institution. I am very grateful to my senior colleagues during postgraduation, Dr Ashesh Wankhede (Professor and Head, Forensic Medicine, Government Medical College, Jagdalpur, Chhattisgarh), Dr Anil Batra (Professor and Head, Forensic Medicine, Government Medical College, Akola) and Dr Kailash Zine (Professor and Head, Forensic Medicine, Government Medical College, Aurangabad) for being the first teachers who taught me medicolegal work. I am also thankful to my classmates Dr Prakash Mohite (Professor and Head, Forensic Medicine, Medical College, Sawangi) and Dr Manish Shrigiriwar (OSD, Super-speciality Hospital, Nagpur) for their constant encouragement and unremitting help. I respectfully thanks to Dr PG Dixit, Professor and Head, Forensic Medicine, Government Medical College, Nagpur, for permitting to carry out this work in the department. I am respectfully thankful to Dr LK Bade, Dr HT Katade, Dr SS Gupta, Dr RK Singh (Raipur), Dr BH Tirpude (Sevagram), Dr SD Nanandkar, Dr SC Mohite, Dr Harish Pathak (Mumbai), Dr VR Agrawal (Pune), Dr HV Godbole, Dr RN Kagne (Pondicherry) for their guidance and blessing. I am grateful to my friend Dr Linesh Khobragade (Consultant Pharmacologist, Sarjah), Dr Satin Meshram and Dr Nilesh Tumram (Department of Forensic Medicine, Government Medical College, Nagpur) without whom this endeavor would not have been possible. I am thankful to Vinia Ambade (BE, Pune), Dr Raj Bhagwatkar (BDS, Nagpur), Dr Avinash Turankar (Department of Pharmacology, Nagpur) and Dr Pravin Shingade (Department of Medicine, Nagpur) for their help while preparing and editing the manuscript. I am also thankful to Dr Hemant Kukde (Mumbai), Dr Nitin Barmate (Raipur), Shri Pramod Mandekar, Mr Sudesh Rathod (Yeotmal), Shri Gurudyal Pathak, Shri Ghodmare (Nagpur), Mr Arun Gujar (Pune), Mr Shantnu Sarkar and Mr Rajesh Shrivas (Nagpur) for their kind help. Finally, I express my sincere gratitude and acknowledgment to my wife Dr Hemlata and lovely daughters Vidhi and Aarohi in accomplishing the task.

Vipul Ambade

Contents Preface to the Second Edition

vii

Preface to the First Edition

ix

1. General Toxicology

1

2. Preservation of Viscera and Other Materials

20

3. Forensic Science Laboratory and Analytical Methods Including Psychoanalysis 40 4. Corrosives

55

5. Mechanical Irritants

67

6. Non-Metallic Inorganic Chemical Irritants

70

7. Irritants: Inorganic Metallic Poison

76

8. Agricultural Poison: Pesticides

91

9. Plant and Vegetable Irritants

108

10. Animal Irritants

117

11. Somniferous Poison: Opium and its Alkaloids

138

12. Inebriant Poison: Alcohols

144

13. Deliriant Poisons: Datura, Cannabis and Cocaine

160

14. Cerebral Depressant

171

15. Cerebral Stimulant

177

16. Hallucinogens

182

17. Spinal Poisons

184

18. Peripheral Nerve Poisons

188

19. Cardiac Poisons

191

20. Asphyxiant and Irrespirable Poisons

198

xii

Forensic Toxicology: A Comparative Approach

21. Drug Dependence and Abuse

206

22. Food Poisoning

214

23. War Gases: Chemical and Biological

223

Appendix

227

Multiple Choice Questions

232

Index

243

Competencies

xiii

Competencies COMPETENCIES RELATED TO TOXICOLOGY FOR COMPETENCY BASED LEARNING AS RECOMMENDED BY MEDICAL COUNCIL OF INDIA FOR MEDICAL GRADUATES Number

Competency: The student shoud be able to

FM2.14

Topic: Forensic Pathology Describe and discuss examination of clothing, preservation of viscera on postmortem examination for chemical analysis and other medico-legal purposes, postmortem artefacts

FM2.19

Investigation of anaesthetic, operative deaths: Describe and discuss special protocols for conduction of autopsy and for collection, preservation and dispatch of related material evidences

FM2.35

Demonstrate professionalism while conducting autopsy in medicolegal situations, interpretation of findings and making inference/opinion, collection preservation and dispatch of biological or trace evidences

FM6.1

Topic: Forensic Laboratory Investigation in Medico-legal Practice Describe different types of specimen and tissues to be collected both in the living and dead: Body fluids (blood, urine, semen, faeces, saliva), skin, nails, tooth pulp, vaginal smear, viscera, skull, specimen for histo-pathological examination, blood grouping, HLA typing and DNA fingerprinting. Describe Locard’s Exchange Principle

FM6.2

Describe the methods of sample collection, preservation, labelling, dispatch, and interpretation of reports

FM6.3

Demonstrate professionalism while sending the biological or trace evidences to Forensic Science laboratory, specifying the required tests to be carried out, objectives of preservation of evidences sent for examination, personal discussions on interpretation of findings

FM7.1

Enumerate the indications and describe the principles and appropriate use for: DNA profiling, Facial Reconstruction, Polygraph (Lie Detector), Narcoanalysis, Brain Mapping, Digital autopsy, Virtual Autopsy, Imaging technologies

FM8.1

Topic: Toxicology: General Toxicology Describe the history of Toxicology

FM8.2

Define the terms Toxicology, Forensic Toxicology, Clinical Toxicology and poison

FM8.3

Describe the various types of poisons and diagnosis of poisoning in living and dead

FM8.4

Describe the Laws in relations to poisons including NDPS Act, Medico-legal aspects of poisons

FM8.5

Describe Medico-legal autopsy in cases of poisoning including preservation and dispatch of viscera for chemical analysis

FM8.6

Describe the general symptoms, principles of diagnosis and management of common poisons encountered in India

FM8.7

Describe simple bedside clinic tests to detect poison/drug in patient’s body fluids

FM8.8

Describe basic methodologies in treatment of poisoning: Decontamination, supportive therapy, antidote therapy, procedures of enhanced elimination

FM8.9

Describe the procedure of intimation of suspicious cases or actual cases of foul play to the police, maintenance of records, preservation and despatch of relevant samples for laboratory analysis.

xiv FM8.10

FM9.1

Forensic Toxicology: A Comparative Approach Describe the general principles of Analytical Toxicology and give a brief description of analytical methods available for toxicological analysis: Chromatography—Thin Layer Chromatography, Gas Chromatography, Liquid Chromatography and Atomic Absorption Spectroscopy Topic: Toxicology: Chemical Toxicology Describe General Principles and basic methodologies in treatment of poisoning: Decontamination, supportive therapy, antidote therapy, procedures of enhanced elimination with regard to: Caustics Inorganic—sulphuric, nitric, and hydrochloric acids; Organic—Carboloic Acid (phenol), Oxalic and acetylsalicylic acids

FM9.2

Describe General Principles and basic methodologies in treatment of poisoning: Decontamination, supportive therapy, antidote therapy, procedures of enhanced elimination with regard to Phosphorus, lodine, Barium

FM9.3

Describe General Principles and basic methodologies in treatment of poisoning: Decontamination, supportive therapy, antidote therapy, procedures of enhanced elimination with regard to arsenic, lead, mercury, copper, iron, cadmium and thallium

FM9.4

Describe General Principles and basic methodologies in treatment of poisoning: Decontamination, supportive therapy, antidote therapy, procedures of enhanced elimination with regard to ethanol, methanol, ethylene glycol

FM9.5

Describe General Principles and basic methodologies in treatment of poisoning: Decontamination, supportive therapy, antidote therapy, procedures of enhanced elimination with regard to Organophosphates, Carbamates, Organochlorines, Pyrethroids, Paraquat, Aluminium and Zinc phosphide

FM9.6

Describe General Principles and basic methodologies in treatment of poisoning: Decontamination, supportive therapy, antidote therapy, procedures of enhanced elimination with regard to ammonia, carbon monoxide, hydrogen cyanide and derivatives, methyl isocyanate, tear (riot control) gases

FM10.1

Describe General Principles and basic methodologies in treatment of poisoning: Decontamination, supportive therapy, antidote therapy, procedures of enhanced elimination with regard to: (a) Antipyretics: Paracetamol, Salicylatess (b) Anti-Infective, (Common antibiotics—an overview), (c) Neuropsychotoxicology: Barbiturates, benzodiazepins; phenytoin, lithium, haloperidol, neuroleptics, tricyclics, (d) Narcotic Analgesics, Anaesthetics, and Muscle Relaxants, ( e ) Cardiovascular Toxicology Cardiotoxic plants—oleander, odollam, aconite, digitalis, (f) Gastrointestinal and Endocrinal Drugs—Insulin

Topic: Toxicology : Pharmaceutical Toxicology

Topic: Toxicology: Biotoxicology FM11.1

Describe features and management of Snake bite, scorpion sting, bee and wasp sting and spider bite

FM12.1

Describe features and management of abuse/poisoning with following chemicals: Tobacco, cannabis, amphetamines, cocaine, hallucinogens, designer drugs and solvent

Topic: Toxicology: Sociomedical Toxicology

Topic: Toxicology: Environmental Toxicology FM13.1

Describe toxic pollution of environment, its medico-legal aspects & toxic hazards of occupation and industry

FM13.2

Describe medico-legal aspects of poisoning in Workman’s Compensation Act

FM14.2

Demonstrate the correct technique of clinical examination in a suspected case of poisoning and prepare medico-legal report in a simulated/supervised environment

FM14.3

Assist and demonstrate the proper technique in collecting, preserving and dispatch of the exhibits in a suspected case of poisoning, along with clinical examination

Topic: Skills in Toxicology

Competencies

xv

FM14.16

To examine and prepare medico-legal report of drunk person in a simulated/supervised environment

FM14.17

To identify and draw medico-legal inference from common poisons: Datura, castor, cannabis, opium, aconite copper sulphate, pesticides compounds, marking nut, oleander, Nux vomica, abrus seeds, Snakes, capsicum, calotropis, lead compounds and tobacco.

PH1.22

Integration Topics Describe drugs of abuse (dependence, addiction, stimulants, depressants, psychedelics, drugs used for criminal offences)

PH5.7

Demonstrate an understanding of the legal and ethical aspects of prescribing drugs

IM20.1

Enumerate the poisonous snakes of your area and describe the distinguishing marks of each

IM20.2

Describe, demonstrate in a volunteer or a mannequin and educate (to other health care workers/ patients) the correct initial management of patient with a snake bite in the field

IM20.3

Describe the initial approach to the stabilisation of the patient who presents with snake bite

IM20.4

Elicit and document and present an appropriate history, the circumstance, time, kind of snake, evolution of symptoms in a patient with snake bite

IM21.2

Enumerate the common plant poisons seen in your area and describe their toxicology, clinical features, prognosis and specific approach to detoxification

IM21.3

Enumerate the common corrosives used in your area and describe their toxicology, clinical features, prognosis and approach to therapy

IM21.4

Enumerate the commonly observed drug overdose in your area and describe their toxicology, clinical features, prognosis and approach to therapy

IM21.5

Observe and describe the functions and role of a poison center in suspected poisoning

IM21.6

Describe the medico-legal aspects of suspected suicidal or homicidal poisoning and demonstrate the correct procedure to write a medico legal report on a suspected poisoning

IM21.7

Counsel family members of a patient with suspected poisoning about the clinical and medico legal aspects with empathy

IM21.8

Enumerate the indications for psychiatric consultation and describe the precautions to be taken in a patient with suspected suicidal ideation/gesture

Reference Medical Council of India, Competency Based Undergraduate Curriculum for the Indian Medical Graduate. Volume-1 (2018). UG-Curriculum-Vol-I.pdf (nmc.org.in)

1 General Toxicology Toxicology is derived from the combination of two words ‘toxic’ from Greek toxikon meaning arrow poison and ‘logy’ meaning study.1,2 The history of poison is as old as human existence. Even in mythological story like Mahabharata, the Pandavas son Bhim was poisoned by Duryodhana. Toxicology is defined as the branch of science which deals with the poisons in all its aspect. Thus, it is the study of poison deals with its source, properties, absorption, fate, action, fatal dose and fatal period, signs and symptoms, laboratory investigation, diagnosis, treatment, postmortem findings and medicolegal aspect of different poisoning cases. Mathieu Orfila is considered as the Father of Modern Toxicology, who has given the subject its first formal treatment in his Traité des poison in 1813.3

Forensic toxicology

Clinical toxicology

It deals with medicolegal aspects of poisoning, including causes and circumstances of death.

It deals with mechanism of action, clinical manifestations, laboratory investigation, diagnosis and treatment of a poison.

Poison

Drugs

• Poison is a substance which when ingested, injected, inhaled, applied or administered causes disease, ill health or death of a person. • It is used to curtail the life or to minimize the life or to get rid of life. • When the substance is given with the intention of causing harm or death, it is considered as poison.

• Whereas, drug is any substance used in the diagnosis, treatment, investigation, and prevention and modification of disease. • It is used to sustain or to prolong life or to get relief. • When a substance is given with the intention of sustaining life, it is considered as a drug, irrespective of the dose.

Legal difference There is no legal definition of poison. Legally the poison and drug are differentiated on the basis of the intention with which that substance is given. Medical difference The difference between the poison and the drug is of dose with which that substance is given. Since a drug in therapeutic dose or lesser dose produces desirable or beneficial effect but the same drug when given in higher dose produces deleterious effect and acts as a poison, e.g. digitalis, barbiturates, diazepam, etc. All drugs are poison when taken in excess dose and with intention to cause harm. But all poisons are not drugs even when taken in low dose.

1

2

Forensic Toxicology: A Comparative Approach

CLASSIFICATION OF POISONS

NATURE OF POISON

Poisons can be classified according to the 1. Action of poison 2. Nature of poison 3. Source of poison

For the medicolegal purpose, poisons are classified as:

ACTION OF POISON

Poisons are classified into 2 groups: (a) Local and (b) Systemic (Table 1.1).

1. Homicidal Poisoning There is no ideal homicidal poison. However, thallium and fluoride (present in rodenticides) are near to ideal homicidal poisons. 4 The commonly used poisons for homicidal purpose are arsenic, aconite, strychnine, snake venom, opium (Table 1.2).

Table 1.1: Classification of poison on the basis of action A. Local

B. Systemic

1. Corrosives 1. Cardiac poisons: Cyanide, aconite, digitalis, a. Acids: tobacco, Cerbera thevetia, Nerium odorum i. Inorganic: Sulfuric acid, hydrochloric 2. Respiratory poisons (asphyxiant gases), e.g. CO, acid, nitric acid CO2, SO2, H2S, NH3, phosphine (PH3), war gases ii. Organic: Acetic acid, oxalic acid, and sewer gases carbolic acid 3. Hepatotoxic poisons: Phosphorus, chloroform, b. Alkalies: trichloroethane, carbon tetrachloride. i. Hydroxide of sodium, potassium and 4. Nephrotoxic poisons: Mercury, carbolic, oxalic, ammonium snake poison ii. Carbonates of sodium, potassium and 5. Miscellaneous: Food poison, drug abuse ammonium c. Metallic: Mercuric chlorides 2. Irritants 6. Neurotics a. Mechanical: a. Cerebral: i. Glass pieces or powder i. Somniferous: Opium and its alkaloids ii. Hairs and fibers like morphine, codeine, thebaine, iii. Metallic chips, nails, pins papaverine, noscapine, and narcine iv. Diamond dust or powder ii. Inebriants: b. Chemical: Alcohols—ethyl and methyl alcohol i. Inorganic Anaesthetic agents: Ether, chloroform, Non-metals: Phosphorus, iodine, nitrous oxide. fluorine, chlorine, bromine Coal tar derivatives, e.g. naphthalene Metals: Arsenic, lead, mercury, copper, iii. Deliriants: Datura, cannabis, cocaine iron, zinc, thallium iv. Depressant (sedatives and hypnotics): ii. Organic: Agricultural poisoning like Barbiturates, benzodiazepam, chloral Insecticidal: Organophosphorus, hydrate, paraldehyde organochlorine, carbamate, pyrethroids v. Stimulants: Amphetamines, camphor, Rodenticidal caffeine, cocaine Fungicidal vi. Hallucinogens: LSD (lysergic acid Herbicidal diethylamide), mescaline (peyote) c. Vegetables: Abrus precatorius, Ricinus communis, b. Spinal: Croton tiglium, Semicarpus anacardium, Calotropis, i. Excitants: Strychnos nux-vomica Plumbago rosea, Capsicum ii. Depressants: Lathyrus sativus (khesari d. Animals: Snakes, scorpions, bees, wasps, daal), gelsemium (jasmine). spiders, cantharides, and poisonous fish c. Peripheral: Conium, curare

General Toxicology

2. Suicidal Poisoning There is no ideal suicidal poison. However, opium and barbiturates are near to ideal suicidal poisons.4 The commonly used poisons for suicidal purpose are insecticides, rodenticides, Table 1.2: Characteristics of an ideal homicidal and suicidal poison Ideal homicidal poison

Ideal suicidal poison

1. 2. 3. 4.

Cheap Easily available Highly toxic Tasteless, odorless, colorless/pleasant Capable of being easily taken with food or drinks Should lead to painless death

5. 6.

7. 8.

Cheap Easily available Highly toxic Odorless, colorless, tasteless Capable of being easily given with food or drinks Produces features that resemble natural disease to avoid suspicion No antidote available Completely metabolised so that it is not detected on TA/PM examination

Not necessary Not necessary

cyanides, carbolic acid, barbiturates, diazepam, opium (Table 1.2). 3. Accidental Poisoning Accidental poisoning can occur due to any poison but commonly occurs due to insecticides, snakebite, and gas leakage from industries. It occurs due to: a. Mistaken with other materials b. Carelessness in storing poisons c. Quack remedies d. While working or exposure in industry, in agricultural fields or in laboratory e. Snakes, scorpions or insects bites f. Leakage of gas from industries g. Accidental consumption of poison by children h. Food poisoning i. Drug overdose or misuse or addiction 4. Other Types of Poisoning on the basis of its Nature (Table 1.3)

Table 1.3: Classification of poison on the basis of its nature Nature of poison Description 1. Homicidal: 2. Suicidal: 3. Accidental: 4. Abortifacients: 5. Aphrodisiac agents: 6. Arrow poisons: 7. Cattle poisons: 8. Stupefying poisons: 9. Malingering purpose: 10. Vitriolage:

3

These are the poisons used for killing other These are the poisons used to commit suicide These are the poisons which cause poisoning due to accidental circumstances These are the poisons used for inducing criminal abortion These are the poisons which increase the sexual desire These are the poisons commonly applied on the arrow head/tip These are the poisons used for killing cattle These are the poisons which alter the consciousness of the person and are commonly given for purpose of rape, robbery, dacoity and theft These are the poisons used for malingering purpose to avoid duty or to make false charges against enemy Agents used to cause bodily injury

Examples Arsenic, aconite, lead, strychnine, etc. Insecticides, cyanides, carbolic, barbiturates, etc. Insecticides, snakebites, food poisoning, gas leakage, etc. Arsenic, lead, ergot, quinine, Calotropis, Plumbago, Nerium, Cerbera thevetia, aconite, strychnine, etc. Alcohol, Datura, cocaine, Cannabis preparations Strychnine, Curare, aconite, Abrus, Calotropis, Plumbago and snake venom Strychnine, Curare, aconite, Abrus, Calotropis, Plumbago, Nerium, Cerbera thevetia Datura, cocaine, Cannabis preparations, alcohol Semicarpus anacardium—branding; Abrus—conjunctivitis Corrosives

4

Forensic Toxicology: A Comparative Approach

Routes of Administration

SOURCE OF POISON

Depending upon the source, poisons are classified as shown in Table 1.4. Table 1.4: Source of poison with its examples Source Examples 1. Domestic/ household

Detergents, disinfectants, phenols, kerosene, etc.

2. Agricultural

Organophosphorus, organochlorine, carbamates

3. Vegetables

All vegetable irritants, Datura, Cannabis, etc.

4. Animals

Snakes venoms, insect bite

5. Medicinal source

Wrong medication, over medication and abuse barbiturate, diazepam, opium, etc.

6. Industrial source

Factories where poisons are produced as by-products, e.g. carbide, methyl isocyanate, phosphine, carbon monoxide, cyanides, etc.

7. Commercial source From storehouse, selling shops, etc. e.g. alcohols, opium, cocaine, etc. 8. Food and drink

Preservatives of foodgrains, additives like coloring and odoring agents, and food poisoning itself

9. Miscellaneous

Sewer gases

PROPERTIES

Color, odor, taste, solubility, form, etc. in relation to particular poison is described in particular chapter. ABSORPTION

The absorption of poison/drug may be direct or indirect through mucous membrane or skin. Direct: Through parenteral routes. Mucous membranes (MM): Sublingual, inhalation, oral and other orifices. Skin: Example phosphorus, phenol, insecticidal poison.

1. Oral 2. Parenteral/injection—SC, IM, IV, intradermal, intra-arterial, etc. 3. Inhalation 4. Sublingual 5. Other natural orifices (e.g. nasal, rectal, vaginal, urethral, etc.). 6. Contact poisoning, i.e. through skin or wounds, or ulcers 7. Through pellets (chemical or bacterial poison pellets fired with airgun). FATE OF POISON

1. Eliminated as such by defecation or vomitus. 2. Neutralized or inactivated in GIT. 3. Metabolized or detoxified in the body. 4. Eliminated after absorption by urine, breath, bile, milk, sweat, saliva, tear, etc. 5. Gets deposited in some organs or tissue. Heavy metals and radioactive substances stored in epidermis, hair, nails and bones and organophosphorus compounds in fat. ACTION OF POISON

The poison may be: 1. Local action: The poison exerts its effect at the site of contact, e.g. corrosive burns with strong acids, dilatation of pupil with atropine, tingling and numbness sensation with aconite. 2. Systemic action: The poison acts on a particular organ/part of the body after absorption of the poison to produce systemic action, e.g. strychnine acts on spinal cord, digitalis acts on heart, curare acts on peripheral nerves, opium/barbiturates acts on CNS. 3. Combined action: Some poisons have both local as well as systemic action after its absorption, e.g. carbolic acid, phosphorus, snake venom. Poison

Local action

Oxalic/carbolic Corrosive Phosphorus Snake venom

Systemic action

Renal and CNS toxicity On GIT Liver and CNS toxicity At the site of bite Also present

General Toxicology

4. General action: The action of poison is not restricted to particular organ but involved multiple system, e.g. metallic poison, insecticidal poison. FACTORS AFFECTING THE ACTION OF POISONS

1. Dose: The action of the poison is directly proportional to its dose. Higher the dose, more will be the fatality and lesser the dose, less will be the fatality with the following exceptions:4 a. Idiosyncrasy: It is the abnormal response of a drug or hypersensitivity due to inborn peculiarities leading to reaction/ death even in a small dose of a drug, e.g. quinine, aspirin, morphine, etc. b. Allergy: It is the hypersensitivity acquired as a result of previous exposure due to the formation of antibodies, e.g. penicillin, NSAID, anti-snake venom. c. Tolerance: It is the capacity of the body to sustain the action of certain drugs or agents without any immediate harm, e.g. alcohol, opium, tobacco, cannabis, etc. The repeated and chronic use of these agents results in addiction and drug dependence. d. Synergism: The final response due to combination of substances is more than the sum of their individual action, e.g. alcohol with cocaine or barbiturates or with antidepressants, anticonvulsants, tranquilizers and antihistaminic. e. Cumulative poisons: Some poisons are not readily excreted from the body and are retained or tend to accumulate in the body and may not cause any toxic effect when ingested/enter the body in a low dose, e.g. lead, arsenic, digitalis, carbon monoxide (CO), strychnine, and barbiturates. 2. Form of poison a. Physical form: The poison in gaseous/ vapor form is more poisonous than liquids, and liquids are more toxic than solids. The solid poison which is in fine

5

powder form is more poisonous than coarse form. [Gases/vapors > liquid > solid (fine > coarse)] b. Chemical form: Pure arsenic and mercury are not poisonous while their compounds are highly poisonous. Similarly, some compound of an individual metal is not toxic and other compound of the same metal is deadly toxic, e.g. barium sulfate is non-toxic and used in barium meal in radiological investigation; whereas barium sulfide is highly toxic. c. Concentrated form: Normally more the concentration, more will be the absorption and more its toxicity. But the dilute solution of oxalic acid is more rapidly absorbed and is much more fatal.5 3. Condition of stomach5: It delays or facilitates the absorption of poison and it depends on: a. Empty stomach—absorbs poison rapidly. b. Food contents in stomach: • Presence of food in the stomach acts as diluents. • Fatty food delays the absorption process of poisoning except phosphorus. c. Abnormal conditions of the stomach also lead to delay in the absorption of poison. • Pyloric stenosis which delays the emptying of food. • Gastrojejunostomy causes repeated backward flow of gastric contents. d. Achlorhydric subjects—the salts of cyanides is ineffective due to lack of hydrochloric acid (HCl) in the stomach which is required for their conversion to hydrogen cyanide before absorption. 4. Routes of administration of poison a. Route: Rate of absorption depends upon the route of administration. Through some routes, poisons are absorbed very rapidly and exert their action promptly. The rate of absorption is fastest through

6

Forensic Toxicology: A Comparative Approach

inhalation routes. This is followed by IV, IM and other parenteral routes as compared to oral and direct skin contact. Injured or ulcerated skin absorbs poison quicker than intact skin. The absorption is more rapid in oral route than rectal route. b. Different route: The action of poisons is different when they are introduced through different routes, e.g. • Snake venom is effective only when injected and harmless when taken orally. • Cocaine: On ingestion acts as deliriants, on injection it acts as local anesthetic. • Curare: On ingestion is inert, on injection it is highly toxic. 5. General condition of the body a. Age: Some poisons are better tolerated in some ages and badly in other ages. Opium is better tolerated by elderly and atropine is better tolerated by children. b. Physique and health: Well-built person with good physique and health will tolerate poison better than weak and lean subject. c. Presence of any disease: Usually, in disease conditions the effect of poison is more. • In liver pathology, Morphine is more poisonous. • In renal damage, Mercury is more poisonous. • In head injury or raised ICP, Morphine is more dangerous/lethal. • However, some poisons are welltolerated during disease conditions like: – Sedatives and tranquilizers in Manic and deliriant patients – Digitalis in heart failure. – Strychnine in paralysis. – Cyanide in achlorhydria. d. Sleep: Absorption is less during sleep due to slow metabolism and hence has slow action but depressant drugs may cause more harm during sleep.

e. Exercise: It decreases the action of drug as more blood is drawn to the muscle, e.g. alcohol. DIAGNOSIS OF POISONING

The diagnosis of poisoning is not always possible due to various reasons. 1. Usually patient is not in a position to narrate the story or to give the history. 2. Sometimes in spite of knowing the nature of poisoning consumed by the patient, the relatives do not come forward due to fear of being involved in police investigation. 3. Also due to ignorance of the importance of giving proper history of poisoning to the doctor, the physician’s task becomes more difficult as none is willing to give correct history to avoid police investigation. 4. Unlike in other clinical conditions arising out of natural disease, there are very few toxic syndrome or toxidrome6 (refer to a group of clinical features that are consistently encountered in relation to a specific toxin) characterized by typical signs and symptoms. In Living Subject 1. History of the case as stated by patient, relatives or friends: It includes time of onset, symptoms, progress, in relation to food/drink and condition of others who took the same, possible source of poison, any past history of poisoning, history of depression and about the properties of the poisonous material like smell, taste, color, consistency, etc. 2. Signs and symptoms of the patient 3. Detailed physical examination 4. Laboratory investigation of vomitus, blood, etc. or any material brought by the relatives. The toxicological analysis (TA) of gastric lavage fluid, blood, urine, stools and vomitus confirms the nature of the poison. The detection of the poison in suspected food, fluid or utensils help as corroborative evidence.

General Toxicology

In Dead Subject 1. History as provided by police or relatives should be taken in the same line as in case of living victims. In addition, history should also contain: i. Period of survival after poisoning and their symptoms. ii. Details of treatment if given. 2. Postmortem examination of a body a. External examination (see page 13): i. Clothes examined for vomitus stain with its color and smell. ii. Body for any injection marks. iii. Mouth and nostrils for presence of froth—in insecticidal poisons, morphine, barbiturates, strychnine and cyanides. iv. PM lividity for peculiar color—in carbon monoxide (cherry red), hydrogen sulphide (bluish green), cyanides (pink) and opium (black lividity). v. Skin for different colors—in acute copper and phosphorous poisoning (yellow due to jaundice) and asphyxiants poisoning (bluish due to cyanosis). vi. Gums and teeth for color changes, particularly in metallic poisons like copper, mercury, lead (bluish color). b. Internal examination (see page 14): i. Organs/viscera should be examined for any congestion and edema. ii. Stomach should be examined for color and smell of its content along with submucosal hemorrhage, softening, congestion and perforations of its wall. In poisoning, these changes are more marked at greater curvature of stomach.4 iii. Small intestine should also be examined for the above changes, particularly in the duodenum and jejunum. 3. Preservation of viscera and other materials for laboratory investigation like TA. 4. Moral and circumstantial evidence in suicidal and homicidal poisoning. i. In suicidal poisoning, it includes suicidal note, cause of suicide with evidence

7

of ingestion/purchase of poison. The container of the poison may be found near the dead body or victim. ii. In homicidal poison, it includes history of quarrel or other cause/motive of homicide with evidence of ingestion/ injection/purchase of poison. The relatives are very eager to dispose of the dead body. TREATMENT OF POISONING

If the specific nature of the poison is not known, then it should be treated on the lines of general principles of treatment of poisoning which are as follows: 1. Removal of patient from the source of exposure 2. Removal of unabsorbed poison 3. Dilution of unabsorbed poison 4. Elimination of absorbed poison 5. Specific antidote 6. Symptomatic treatment However, Stabilization and Evaluation of the patient should be done before starting the actual treatment like decontamination (removal of unabsorbed poison), poison elimination (by means of diuresis, dialysis) and specific antidote administration.6 Stabilization refers to correction of life-threatening problems like airway, breathing, circulation and CNS depression. Evaluation includes complete assessment/examination and diagnosis/laboratory investigation of the patient of poisoning. Moreover, most poisoned patients can be treated successfully without any contribution from the laboratory other than routine clinical biochemistry and hematology investigations. 1. Removal of Patient from the Source of Exposure • In gaseous/volatile poison—remove patient from the source or environment. • In insecticidal poison—removal of clothes. • In corrosives poison—removal of soiled clothes.

8

Forensic Toxicology: A Comparative Approach

2. Removal of Unabsorbed Poison It depends upon the route of administration of poison. a. In case of contact poisoning to skin/ injuries: • Removal of clothes. • Wash the area with lukewarm water or soap. • Application of local anesthetic agents. b. In case of intravaginal or other natural orifices: • Vaginal douching or irrigation with plain water. c. Inhaled poison:

Table 1.5: Contraindications of emesis7 [5CVP-M] Conditions

Reasons for contraindication

a. Corrosive poisoning7 Perforation of the stomach b. CNS stimulant drugs Convulsions may be poisoning7 precipitated c. Kerosene/volatile Chances of aspiration/ poisoning inhalation of fumes d. Morphine poisoning7 May fail to act e. Coma7 Aspiration f. Children Aspiration g. Pregnancy Abortion h. Cardiorespiratory Heart failure may be diseases precipitated

Methods of Emesis Vomiting can be induced by different methods as shown in Table 1.6.

• Removal of patient from source.

Table 1.6: Method of induction of vomiting

• Ensure clear airway and respiration.

a. Mechanical irritation of throat b. Plain lukewarm water c. Common salt d. Mustard powder e. Copper sulfate f. Ipecacuhana syrup g. Zinc sulfate h. Ammonium carbonate i. Apomorphine hydrochloride

d. Injected poison (e.g. snakebite, arrow poison): The spread of injected poison is restricted by: • Application of ligature/tourniquette proximal to the site of bite. • Application of ice packs. • Antidote infiltration after washing of the site of bite. e. Ingested poison: The ingested poison is removed by: • Emesis/induction of vomiting. • Gastric lavage/stomach wash. • Purgatives and colonic lavage by means of sodium/magnesium sulfate or dulcolax, etc. Emesis Emesis means induction of vomiting. It is better than stomach wash within 4–6 hours of ingestion of poisoning. It is absolutely contraindicated in all corrosive poisoning except carbolic acid. In rest of the condition, it is relatively contraindicated (Table 1.5).

Finger—stimulating the posterior wall of pharynx Good amount of water 1 TSF in one glass of water 1 TSF in one glass of water Weak solution 15–30 ml orally7 1–2 gm in one glass of water 1–2 gm in one glass of water 6 mg IM/SC7, is centrally acting potent emetic agent.

Household emetics: These are the emetics available in the house. Top four methods are the examples of household emetics. Gastric Lavage Gastric lavage/Stomach wash is the cleaning of the stomach with fluid. The volume of each wash depends on the age group of the person. It is done by means of following gastric lavage tubes: In age group

GL tube

Volume of each wash

Adults

Stomach tube (Boa’s/Ewald’s)

200–300 ml

Children

Male urinary rubber catheter

100–200 ml

Infants

Ryle’s tube

300 ml of either plain water or KMnO 4 solution (1 : 1000) or with specific antidote to particular poison. This process of entry and removal of fluid from the stomach is

10

Forensic Toxicology: A Comparative Approach

repeated till the color of lavage fluid remains same. At the end, the tube is removed properly to avoid aspiration of fluid to respiratory tract by pinching or bending between the finger.4 However, in certain cases, the lavage fluid (KMnO4 solution) is left in the stomach to neutralize the un-removed part of the poison, if any. The fluid (KMnO4 solution, activated charcoal, demulcent) can also be left in certain poison that may be re-secreted in stomach (e.g. morphine) or that remains adherent to gastric mucosa. 3. Dilution of Unabsorbed Poison It is done by giving: a Water to drink that helps in two ways: • It reduces the local damaging action • It delays the rate of absorption b. Bulky bland food, e.g. banana, boiled potato, mashed rice. c. Demulcents/fats: It delays the process of absorption and also protects the stomach wall. This method is of no use in oxalic acid poisoning (where dilution is contraindicated), and phosphorus poisoning (where fats are contraindicated). 4. Elimination of Absorbed Poison It is done by: a. Diuresis (increased urination/forced diuresis) by using fluids and drugs like frusemide or mannitol infusion. b. Diaphoresis (increased sweating/perspiration) by applying hot packs and neostigmine or pilocarpine injection. c. Dialysis: In case kidney is not functioning (peritoneal or hemodialysis). d. Chelating agents: See antidotes e. Exchange transfusion: Capable of removing many of the toxins that are not removed by hemodialysis. It is best indicated in cerebral depressant, cardiac poison (digoxin, quinine), organophosphorus, phenol, paraquat, paracetamol, amanitin poisoning.6

5. Specific Antidote Antidote is the substance which counteracts the deleterious effects of the poison without itself being harmful to the body. It is indicated when poison is absorbed from the GIT or shows clinical systemic manifestation of poison (see Appendix Table 1). Types and Uses of Antidotes

I. Physical (mechanical) antidotes: These are the antidotes which prevent the action of poison mechanically without destroying or neutralizing the poison. Different physical antidotes with their examples and uses are given in Table 1.8. II. Chemical antidotes: These are the substances which chemically react with the poison and thereby disintegrate or inactivate the poison (Table 1.9). III. Pharmacological or physiological antidotes: These are the substances which have a pharmacologically opposite action as compared to the poison (Table 1.10). IV. Universal antidote: It is so-called because it can be used in all cases of poisoning, especially when the nature of poison is not known. It is the combination of physical and chemical antidotes (Table 1.11). Dose is 15–30 g or 1 TSF in a glass of water.5,13 It can be repeated 12–24 hourly. It is nowadays obsolete but can be used as first aid measure at home.12–13 V. Chelating agents: These are the substances which act on the absorbed metallic poison and form a non-ionized complex with the metal ion freely available in the blood circulation, so that the metal ion is not available for absorption and thereby cannot affect the enzyme system of the body. The commonly used chelating agents are BAL, EDTA, Penicillamine, and Desferrioxamine (Table 1.12). VI. Serological/biological antidotes: These are the substance prepared by injecting the antigen (like snake venom) in the animal blood, so that the sensitized animal serum can be used as an antidote, e.g. antivenom serum.

General Toxicology

11

Table 1.8: Different types of physical antidotes Physical antidote

Examples

Action/properties

Uses

Demulcent

Oil, ghee, butter, milk, egg albumin (egg white), starch, barley, water, etc.

These substances have soothing action and form a protective layer on the mucosa of stomach so that the poison does not absorb

Corrosive/irritant, except phosphorus

Bulky foods

Banana, mashed potato, boiled rice, vegetables, etc.

These substances engulf the poison and make it unavailable for causing effects and for its absorption

Mechanical irritant

Adsorbent

Activated charcoal (dose: 1 gm/kg body weight12 in water orally)6

It adsorbs the alkaloid poison in their pores so that poison is not available for absorption in stomach

Irritant poison

Diluents

Water, milk, drinks, etc.

It dilutes the poison, thereby delaying the absorption of poison

Corrosive/irritant, except oxalic acid

Table 1.9: Chemical antidotes and their uses Chemical antidote

Uses (action/forms)

a. Weak non-carbonated alkali5 (CaO, MgO) b. Weak vegetables acid5 (citric, acetic) c. Copper sulfate d. Egg albumin e. Fresh ferric oxide f. Potassium ferrocyanide g. Calcium carbonate h. KMnO4 i. Sodium thiosulfate

Acid poison (neutralizing the acids) Alkali poison (neutralizing alkali) Phosphorus (forms copper phosphide) Mercury chloride (forms mercuric albuminate) Arsenic (forms ferric arsenate) Copper Oxalic acid (forms calcium oxalate) Opium/morphine Iodine/cyanide

Table 1.10: Pharmacological antidotes and their uses Pharmacological antidote

Dose8-11

Physostigmine/Neostigmine8

0.5–2 mg IV

Datura, atropine

Atropine8

2 mg IV repeated every 10 min till dryness of mouth

Organophosphorus (OP)

Ethanol9

0.7 ml/kg through nasogastric tube followed by 0.15 ml/kg/hour

Methanol

Naloxone10

0.4–0.8 mg IV every 2–3 min (max 10 mg)

Opium/morphine

Lorazepam11

4 mg IV, repeated after 10 min if required

Strychnine

Uses/for

Table 1.11: Content of universal antidote Contents

Obtained from4

Parts

Action

Charcoal MgO Tannin

Burnt bread/toast Milk of magnesia Strong tea

2 1 1

Adsorbs poison Neutralizes acid Precipitates metal, alkaloids, and glucosides

12

Forensic Toxicology: A Comparative Approach

Table 1.12: Examples of chelating agents with their dose and uses Chelating agents Properties

Dose

Adverse effects

Uses14

a. BAL It is an oily, pungent, (Dimercaprol) viscous liquid developed during World War II as an antidote to the arsenical war gas lewisite. It has 2 SH groups which bind with metal ion present in the blood.14

5 mg/kg body weight stat deep IM followed by 2–3 mg/kg 4–8 hourly for first 2 days, followed by 12 hourly (1BD) for next 10 days.14 If given IV, it causes embolism due to presence of arachis oil in benzyl benzoate.

Hypertension, tachycardia, sweating, cramps, headache, anxiety. It is CI in iron and cadmium poisoning; and in G6PD deficiency12

• Arsenic, mercury poisoning • Bismuth, nickel, gold, antimony. • Adjuvant to copper poisoning and Wilson disease. • Adjuvant to calcium disodium edetate in lead poisoning.

Dimercaptosuccinic acid: It is less toxic and effective orally for lead poisoning. b. Calcium disodium edetate (CaNa2 EDTA)

It has higher affinity for metals like Pb, Zn, Cd, Mn, Cu and some radioactive metals by exchanging with calcium present in it.14

1 gm in 200–300 ml saline/glucose by slow IV drip, BD for 3–5 days. Repeated after 5–7 days14

• As, Hg, Pb poisoning Renal damage • Lead poisoning with proximal • Cu, Fe, Zn, Mn but not tubular necrosis, in mercury poisoning. acute febrile reaction, anaphylaxis

The disodium salt of ethylene diamine tetraacetic acid (Na2 EDTA) is a potent chelator of calcium, it causes tetany. Dose: 50 mg/kg IV infusion for 2–4 hrs.14

• Emergency control of Hypercalcemia

c. Penicillamine It is a degradation product of penicillin. It has stable SH-radicle. It selectively chelates Cu, Hg, Pb and Zn. It is adequately absorbed after oral administration.

30 mg/kg body weight, orally in 4 divided doses for 7 days.5 OR 0.5–1 g/day orally in divided dose for few days 1 hr before meals 14 OR Potassium sulfide 20–40 mg to reduce absorption of dietary copper 14

Usually nontoxic but may cause thrombocytopenia, skin rash, renal problems.

• Copper poisoning • Wilson disease • Alternative to dimercaprol for Hg poisoning • Adjuvant to CaNa2 EDTA in lead poisoning. • Cystinuria and cystine stones

d. Desferrioxamine

0.5–1 g/day IM, repeated 4–12 hourly till serum iron falls below 300 microgram/dl.14 OR 10 g/day orally for unabsorbed iron.5

It releases histamine and causes skin lesion. Also causes cramps, abd pain, loose motion, fever.

• Iron poisoning. • Transfusion siderosis in thalassemia patients. (BAL is not given in iron poisoning)

Chemical removal of iron from Ferrioxamine yields desferrioxamine which has very high affinity for iron.14

Deferiprone: It is an orally active iron chelator particularly in transfusion siderosis and alternative to iron poisoning. Dose: 50–100 mg/kg daily in 2–4 divided doses.14

Household Antidotes These are the substances which are available usually in the house and can be used as antidotes in case of poisoning (Table 1.13)

General Toxicology Table 1.13: Household antidotes and their uses Household antidotes 1. Common salt, mustard powder, plain warm water 2. Charcoal from burnt toast 3. Flour suspension 4. Banana, potato, boiled rice 5. Oil, ghee, butter, milk, egg albumin 6. Starch solution 7. Milk of magnesia, tooth paste, wall scrapping 8. Vinegar, lemon/orange juice 9. Milk 10. Strong tea (Tannic acid)

Uses/used as Emetic agent Adsorbent Engulf or even adsorb Physical antidote Demulcent Iodine poisoning Acid poisoning Alkali poisoning All ingested poison Metallic poison, cocaine, nicotine, strychnine13

6. Symptomatic Treatment A. Safeguarding respiration 1. Clearing the airways 2. Endotracheal intubation 3. Tracheostomy 4. Oxygen inhalation—6 liters/min 5. Artificial respiration B. Maintenance of circulation 1. Vasoconstriction 2. Stimulants 3. Blood transfusion 4. Noradrenaline drip for peripheral circulatory failure C. Electrolyte imbalance correction 1. IV fluids for dehydration/shock 2. Sodium/potassium for electrolyte imbalance 3. Other fluids D. Other supportive treatments like 1. Atropine for abdominal pain 2. Diazepam for convulsions/restlessness 3. Adrenaline, antihistaminic and steroids in anaphylactic reactions 4. Morphine, pethidine for pain 5. Glucose for hypoglycemia E. Maintenance of general condition of the patient 1. Warm and comfortable condition 2. Good nursing care 3. Prophylactic antibiotics 4. Physiotherapy for rehabilitation 5. Psychotherapy in an attempted suicide

13

POSTMORTEM FINDINGS IN SUSPECTED POISONING

The postmortem (PM) findings are different in individual poisoning which are described in respective chapters. However, the characteristic findings in different poisoning are as follows: External Postmortem Findings 1. Postmortem lividity: Deep blue color Asphyxiant/aniline Cherry-red CO poisoning Pink Cyanide Brown Phosphorus Black Opium Green Hydrogen sulfide 2. Froth from mouth and nose 3. Detectable smell

Opium, barbiturate, Cyanide, strychnine, OP (blood tinged) Insecticidal poison, volatile poison, opium, cyanide, kerosene, phenol Opium, CO2, sewer gas, Strychnine, HCN Arsenic, datura, formalin Nitric acid, copper sulfate, paints Corrosives

4. Deep cyanosis 5. Early rigor mortis 6. Resist decomposition 7. Stain near mouth and on hands 8. Ulceration on lips and mouth 9. Hemorrhage spots Phosphorus under skin/mucosa 10. Staining, erosion, Abortifacient agents, ulceration near corrosives external genital5 11. Alopecia, Arsenic hyperpigmentation, hyperkeratosis5 12. Injection marks Opium/cocaine abuser 13. Punctures marks Bite marks of snakes, scorpion and insect 14. Constriction of Morphine, phenol, pupil organophosphorus, 15. Dilatation of pupil Datura, alcohol

14

Forensic Toxicology: A Comparative Approach

Internal Postmortem Findings 1. Corrosion, Corrosive ulceration and desquamation of lips, mouth, tongue5 2. Soft, swollen, Alkali bleached (whitish or yellowish) tongue/mouth5 3. Chalky white teeth Sulfuric acid 4. Blue lining on Lead, mercury gums/teeth (chronic poisoning) 5. Corrosion, Corrosives, irritant ulceration and desquamation of GIT mucosa 6. MM of upper GIT Hard/white Phenol Yellow Nitric acid Bluish green Copper sulfate Green Ferrous sulfate Black Sulfuric acid Grey/slate color Mercury chloride Red velvety Arsenic Discolor/staining Colored salts of arsenic, lead, copper 7. Stomach wall Thickened and soft Corrosive, irritant Hard wall Formaldehyde Hard and leather- Carbolic acid like Hemorrhage/ Irritant ulcerated Ulceration and Corrosive sloughing 8. Stomach contents Blood Corrosive, irritant Bluish Copper sulfate Luminous in dark Phosphorus Powder/tablets Drug tab, arsenic, oxalic Detectable smell Kerosene, alcohol, insecticides, cyanide, formaldehyde, etc.

9. Small intestine: May show irritation, corrosion, ulceration as similar to stomach with presence of poisonous remains. 10. Large intestine: May show corrosion, ulcerations in strong acid ingestion. It particularly involves the ascending and transverse colons. 11. Brain and spinal cord: Brain may be congested, oedematous in cerebral poison with occasional hemorrhagic points at places in asphyxiant poisons. In spinal poison, spinal cord is congestion and edematous. 12. Larynx and trachea: Froth may be present in opium and OP poisoning. It is inflamed and hyperemic in inhalation of irritating gases/acid fumes or aspiration of acids. 13. Chest cavity: Smell of volatile poisons, cyanide, opium, etc. can be detected. 14. Lungs: It may be voluminous, congested and may show Tardieu’s spots in asphyxiant poisons. Cut section gives bloodstained frothy fluid in opium and asphyxiant poison. 15. Heart: Subendocardial hemorrhagic spots in poisoning with arsenic, phosphorus, mercuric chloride, etc. 16. Liver: Different degenerative changes may be present in poisoning with phosphorus, carbon tetrachloride, chloroform, tetrachloroethylene, etc. 17. Kidneys: Swollen, reddish, soft, sometimes greasy in touch with hemorrhage in the calyces and other degenerative changes in poisoning with mercury, oxalic acid, carbolic acid, phosphorus, viper snakebite, etc. In case of oxalic acid poisoning, white oxalate crystals are present in the tubules and the calyces. 18. Uterus and vagina: Staining, congestion, hemorrhage, ulceration in attempted abortion by use of local abortifacient agents. DUTIES OF DOCTOR IN POISONING CASES

1. Treatment: The primary duty of a doctor is to treat the patient in any case. If the

General Toxicology

nature of poison is unknown, then the patient should be treated on general principle of treatment of poisoning. 2. History in details of the case: The information about poison with respect to its type, nature, color, smell, etc. should be recorded along with amount/time of consumption of the poison and motive/ reason of poisoning. Details about time of onset and nature of manifestation should also be recorded along with its history of vomiting if any with its nature, smell and color. 3. Informed to authorities: • The doctor must inform to police in all cases of poisoning irrespective of whether it is suicidal or homicidal or accidental poisoning. • If the patient is about to die, then arrange for dying deposition or dying declaration. • If the patient dies, police must be informed and the body should be sent for postmortem examination. • In case of accidental poisoning due to food/water, public health authorities should also be informed so that precautions can be taken for public health safety. 4. Maintenance of BHT records: The record is very important for future reference if required to produce in the court/police. Detailed information of the complaint, condition and treatment of the patient should be included in the record. Details about name, age, sex, address, brought by, consent and identification marks of the patient should also be included in the record. The bed head ticket (BHT) record (case paper of the patient) should be prepared meticulously and updated on daily basis. It should be numbered serially before submitting to record section of the hospital. 5. Preservation of material for toxicological analysis: A doctor must preserve all possible evidence of suspected poisoning. He should preserve stomach wash, vomitus,

15

urine, blood and also other suspicious articles and utensils used in poisoning. POISONING AND LAW

1. If the patient of poisoning is brought dead, then doctor should inform the police and send the body for postmortem examination. 2. The doctor is bound to inform to police in poisoning cases irrespective of whether it is suicidal or homicidal or accidental poisoning. As per Sec 39 of CrPC, it is mandatory for a doctor to inform the police for the commission of homicidal poisoning. 3. The doctor has to preserve all possible material/evidence of suspected poisoning. The doctor is bound to provide all information/documents to the police/ court in poisoning cases when asked or summoned. If the doctor causes any evidence to disappear or gives false information with the intention of screening the offender is punishable u/s 201 IPC; and if he intentionally omits to give any information relating to poisoning is punishable u/s 202 IPC. Whoever gives any false evidence in any stage of judicial proceeding is punishable u/s 193 IPC. 4. Indian penal code also describes the punishment specifically related to the poisoning and adulteration to deal offences related to drugs and poison (Table 1.14). ACTS RELATED TO THE USE OF DRUGS AND POISON

In India, dealing of poisons and drugs are governed by Acts which are as follows: 1. The Opium Act, 1857: This Act empowers the Central Government to cultivate poppy plants and manufacture opium in the farms authorized by the Government. This Act was amended in 1878. 2. The Opium Act, 1878: This Act prohibits transport, possession and sale of opium. This Act was further amended in 1957.

16

Forensic Toxicology: A Comparative Approach

Table 1.14: Punishment for offence related to drugs and poison Sec of IPC

Offence

Punishment

272

Adulteration of food or drink intended to sell, so as to make it noxious

Imprisonment of either description for a term which may extend to 6 months and/or fine of up to `1000

273

Sale of noxious food or drink

Imprisonment of either description for a term which may extend to 6 months and/or fine of up to `1000

274

Adulteration of drugs with any changes in its effect intended to sold or use

Imprisonment of either description for a term which may extend to 6 months and/or fine of up to `1000

275

Sale of adulterated drugs

Imprisonment of either description for a term which may extend to 6 months and/or fine of up to `1000

276

Sale of drug as a different drug or preparation

Imprisonment of either description for a term which may extend to 6 months and/or fine of up to `1000

277

Fouling water of public spring or reservoir

Imprisonment of either description for a term which may extend to 3 months and/or fine of up to `500

278

Voluntarily making atmosphere noxious

Fine which may extend to `500

284

Negligent conduct with respect to poisonous substance so as to endanger human life or likely to cause hurt or injury

Imprisonment of either description for a term which may extend to 6 months and/or fine of up to `1000

326A

Voluntarily causing grievous hurt by use of acid

Imprisonment of either description for a term which may not be less than 10 years but may extend to imprisonment of life and fine

326B

Voluntarily throwing or attempting to throw acid on any part of the body with an intention of causing damage or disfigurement

Imprisonment of either description for a term which may not be less than 5 years but may extend to 7 years and fine

328

Causing hurt by means of poison or any intoxicating agent or drug with intent to commit an offence

Imprisonment of either description for a term which may extend to 10 years and fine

3. The Poisons Act, 1919: This Act deals with the regulation of import of poisons and grant of license for the possession and sale of poisons. 4. The Dangerous Drugs Act, 1930: This Act regulates the import, export, cultivation, manufacture, possession, sale and use of dangerous drugs of abuse like opium, cannabis and cocaine. 5. The Drugs Act, 1940: This Act regulates the import, manufacture, distribution and sale of drugs in India. This Act was amended in 1962 to include cosmetics

under its purview. It is now known as “Drugs and Cosmetics Act of 1940”. 6. The Drugs and Cosmetics Act, 1940: This Act empowered the Central Government to form a Drugs Technical Advisory Board, and to establish a Central Drugs Laboratory, to help and advice the Governments for enforcing uniformity in the implementation of the different provisions of the Act, all over the Country. The Central Drug Laboratory analyses the purity and potency of imported and manufactured drugs. This Act was further amended to include Ayurvedic

General Toxicology

and Unani drugs under its purview in 1964. 7. The Drugs and Cosmetics Rules, 1945: The rules were framed under the provisions of the Drugs and Cosmetics Act of 1940 (former Drugs Act of 1940), which came into effect in 1945, known as Drugs and Cosmetics Rules of 1945, to regulate the import, manufacture, distribution and sale of drugs and cosmetics. Under these rules, drugs are classified in certain schedules as follows: Schedule C: Biological and special products; Schedule E: List of poisons, Schedule F: Vaccines and sera, Schedule G: Hormone preparation, Schedule H: Poisonous drugs which cannot be sold without a prescription, Schedule J: List of drugs used to cure disease which should not be advertised, and Schedule L: Antibiotics, antihistaminics and other chemotherapeutic agents. [Schedule H and L drugs cannot be sold without the prescription.] This rule also dictates the procedure of sale of medicine by the retailer. The retailer should maintain a register, which should contain the name and address of patient and prescribing doctor, name and ingredients of drug, the serial number and date of the sale should be recorded along with the name of manufacturer, batch number of the product and the expiry date of the drug enlisted in Schedule C, H and L.5 8. The Pharmacy Act, 1948: It regulates the Pharmacy Councils and allows only the registered pharmacist to compound, prepare, mix or dispense any medicine on the prescription of doctor. 9. The Drugs Control Act, 1950: It regulates the sale, supply, distribution and regulates the maximum price of a drug.

17

10. The Drugs and Magic Remedies Act, 1954: It bans the advertisement of magic remedies in relation to: (i) abortion, (ii) prevention of conception, (iii) increase sexual potency/ pleasure, (iv) treatment for menstrual disorders, (v) treatment and cure of venereal diseases, (vi) false or misleading information about a drug as to its nature and function. 11. Medicinal and Toilet Preparation Act, 1955: This Act provides for payment of levy and excise duty for medicinal and toilet preparations containing alcohol, cannabis, opium and other similar drugs.5 12. Narcotic Drugs and Psychotropic Substances Act, 1985: It repeals three Acts, namely The Opium Act, 1857 and 1878; and the Dangerous Drugs Act, 1930. This Act i. Consolidates and amends the existing laws relating to narcotic. ii. Strengthens existing control over drug of abuse. iii. Makes stringent provision for the purpose of preventing, combating trafficking, and abuse of narcotic drugs and psychotropic substances. To enforce the Act, Government of India had framed ND and PS Rules, 1985. Likewise, State Governments have also formed their own rules to enforce this Act within their jurisdiction. A narcotic drug is one that produces narcosis or sleep. A narcotic drug includes cannabis, cocaine, opium, and their derivatives. Psychotropic drugs are one that alters mental function by its action. “Psychotropic substances” means any substance or preparation of such substance that are included in the list of 77 psychotropic substances, e.g. hallucinogens—LSD, stimulants—amphetamines, hypnotic—barbiturate, tranquilizer— diazepam, meprobamate. The Act prohibits the cultivation of poppy, cannabis and coca plants; however restricted cultivation is allowed for medicinal purpose. This Act also provides punishment of imprisonment for those dealing in these

18

Forensic Toxicology: A Comparative Approach

drugs and substance, for 10 years which may extend to 20 years with fine of ` 1 lakh extend to 2 lakhs. Under Section 27, person who is found to be in possession of a small quantity of any drugs or substance for his personal use or who consume any material under this Act is punishable for a period of one year with fine or both. IMPORTANT QUESTIONS

1. Classify poisons on the basis of their action. Describe general principles of treatment of poisoning. 2. Classify poison according to mode of poison. Enumerate the poisons which discolor/impart color to the skin and mucous membrane. 3. Write different actions of poison. Describe factors affecting absorption of poison. 4. Define antidote. Describe different types of antidote with their examples. 5. Write in brief about chelating agents with examples as an antidote. 6. Write indication and contraindication of emesis and stomach wash. Describe the procedure for stomach wash. 7. Describe the duties of doctor in case of poisoning. 8. Describe general guidelines or steps for diagnosis of poisoning in general. 9. How will you diagnose a case of poisoning during postmortem examination? What are the reasons for negative report from chemical analyser in a suspected case of poisoning? 10. A patient is brought in the hospital / casualty in an unconscious condition with history of poisoning. Discuss differential diagnosis and briefly outline the management in anyone of them. SHORT NOTES/SAQs

1. Stomach tube 2. Laws related to poisons

3. Household emetics 4. Chelating agents 5. Universal antidote 6. Characteristic features of ideal suicidal and homicidal poisons 7. Physical antidotes with its examples, action and uses SPECIFIC LEARNING OBJECTIVES After reading this chapter, the reader should be able to:

• Define toxicology and related terms like poison and drugs • Classify poisons with examples • Enumerate the characteristics of ideal suicidal and homicidal poisons and their examples • Understand different factors affecting the action of poisons • Diagnose poisoning in living and in dead subject • Understand the general principles of treatment of poisoning • Recognize different antidotes and their examples • Enumerate various indication and contraindication of emesis/ gastric lavage and to describe its procedure • Enlist the examples of household emetics/ antidotes • Enlist different chelating agents with their examples, dose and uses • Enumerate different postmortem findings in suspected case of poisoning • Understand the duties of doctor in poisoning cases References 1. Toxicology. www.dictionary.com>browse> toxicology. Assessed on dated 5-11-17. 2. Origin and meaning of toxicology. https:// www.etymonline.com>word>toxicology. Assessed on dated 5-11-17. 3. Biography of Mathieu Orfila (1787-1853). US National Library of Medicine. https:en.m. wikipedia.org>Toxicology. Assessed on 5-11-17.

General Toxicology 4. Singhal SK. Singhal’s Toxicology at a glance. 9th edn, National book depot, Mumbai. 2016: 1–24. 5. Nandy A. Principles of Forensic Medicine. New Central Book Agency (P) Ltd: Calcutta, 2nd edn Reprint, 2004: 438–53. 6. Pillay VV. Textbook of Forensic Medicine and Toxicology. Paras Medical Publisher: Hyderabad, 17th edn, 2016: 470–96. 7. Tripathi KD. Antiemetic, prokinetic and digestant drugs. In: Essential of Medical Pharmacology. 7th edn, Jaypee Brothers Medical Publishers (P) Ltd: New Delhi, 2014: 661–2. 8. Tripathi KD. Cholinergic system and drugs. In: Essential of Medical Pharmacology. Jaypee Brothers Medical Publishers (P) Ltd: New Delhi, 7th edn, 2014: 110–1. 9. Tripathi KD. Ethyl and methyl alcohols. In: Essential of Medical Pharmacology. Jaypee Brothers Medical Publishers (P) Ltd: New Delhi, 7th edn, 2014: 395.

19

10. Tripathi KD. Opioid analgesic and antagonists. In: Essential of Medical Pharmacology. Jaypee Brothers Medical Publishers (P) Ltd: New Delhi, 7th edn, 2014: 483. 11. Tripathi KD. CNS stimulants and cognition enhancers. In: Essential of Medical Pharmacology. Jaypee Brothers Medical Publishers (P) Ltd: New Delhi, 7th edn, 2014: 486. 12. Bardale R. Principles of Forensic Medicine a n d Toxicology. 1st edn, Jaypee Brothers Medical Publishers (P) Ltd: New Delhi. 2011: 413–31. 13. Dikshit PC. Textbook of Forensic Medicine and Toxicology. 2nd edn, PEEPEE Publishers and Distributors (P) Ltd. New Delhi. 2014:451– 73. 14. Tripathi KD. Chelating Agents. In: Essential of Medical Pharmacology. Jaypee Brothers Medical Publishers (P) Ltd: New Delhi, 7th edn, 2014: 905–8.

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Forensic Toxicology: A Comparative Approach

Preservation of Viscera and Other Materials

2

In poisoning deaths, gastric content/viscera or blood is routinely preserved for toxicological analysis to know the type of poison. In some medicolegal case, the cause of death is not clear at autopsy and the viscera and blood is preserved for analysis to give a final opinion. Even in antemortem cases, the sample (like blood or stomach wash) is preserved to estimate the level of intoxicant. Apart from such routine poisoning cases, the viscera and other materials like skin, hair, tissue, bones, urine, blood, etc. are preserved in different cases for various reasons. So, the present chapter includes the preservation of samples/materials in different medicolegal cases like firearm, burns, drowning, hanging, disputed paternity, sexual offences, etc. apart from the poisoning cases. It also includes about preservation of tissue/material for biochemical, serological, microbiological, histopathological investigation and museum purpose.

The viscera and other material from the human body may be preserved for the following reasons/purposes: a. Toxicological analysis (TA)—in poisoning, alcoholic intoxication, drug overdose. • Detection of toxin—in food poisoning b. Blood grouping—in homicidal cases, sexual offences. c. Biological/immunological study—in snakebites. d. Detection of petroleum products—in burns. e. Detection of residual and other material— in cases of firearm. Comparison of ligature fibres—in hanging/strangulation cases. f. DNA fingerprinting—in disputed paternity and other cases. g. Fingerprinting—in unknown persons for identification. h. Diatoms detection—in drowning. i. Biochemical estimation of certain elements and enzymes in poisoning (OP compounds), pathological condition and for time since death. j. Microbiological examination: Culture and sensitivity in infections condition. Bacterial/ protozoa detection in gastroenteritis and cholera.

k. Histopathological examination. l. Histochemical examination. m. Bone examination. n. Wet specimen for museum purpose. INDICATIONS OF VISCERA PRESERVATION FOR TOXICOLOGICAL ANALYSIS (TA)1, 2

1. The doctor conducting the autopsy suspects poisoning. 2. The cause of death is not known at autopsy or where death occurred in suspicious circumstances all of a sudden. 3. The cause of death is established but there is also suspicion of poisoning. 4. The investigating officer requests for the same. 5. In traffic accidents especially of the driver when suspicion of alcohol consumption (blood for TA). 6. In homicidal deaths, to rule out any intoxication. PRESERVATION OF ROUTINE VISCERA

In most of the poisoning cases, the poison is taken orally. It absorbs through stomach and intestines, metabolized in liver and excreted 20

Preservation of Viscera and Other Materials

through kidneys in urine. Thus, the following viscera are routinely preserved at autopsy3,4 (Table 2.1 and Fig. 2.1). V1: Bottle No. 1: Stomach and intestinal loop and their contents. V2: Bottle No. 2: Pieces of liver, ½ of spleen and ½ of both kidneys. V3: Bottle No. 3: Blood 100 ml for TA. Gallbladder should be preserved along with liver since majority of the drugs can be detected in it. Half of each kidney has to be preserved, as one kidney may be non-functional. Sometimes gastric content, urine, vomitus and other materials are also preserved for toxicological analysis. These materials are sent to regional Forensic Science Laboratory (FSL) by the autopsy/treating doctor through the concerned police along with the related prescribed forms duly filled, signed and sealed. Blood for grouping:5 2 ml blood from heart in 2 ml of 5% sodium citrate solution. However, it is preferred to prepare two blood stains of 5 cm diameter on sterile starch free cotton

21

Fig. 2.1: Routine viscera for TA

cloth and send in an envelope after complete air drying. Starch from the cloth is removed by successive washing with plain water and then drying. In routine practice, the stain for grouping is prepared over piece of cotton bandage. Dried blood stain over body for grouping: It is collected by taking stain scrapping if possible or transfer the dried stain onto the clean cotton cloth piece moistened with normal saline or distilled water, by gentle rubbing and send in an envelope after complete air drying.

Table 2.1: Guidelines for preservation of routine viscera in poisoning for TA 3,4 Viscera

Quantity

Preservatives

1. V1: Stomach with its contents + intestinal loop with its contents

Whole stomach with 300 ml or whole, if less is available 1 meter (2 meters in children, whole in infants) 100 ml or whole if less is available

Saturated solution of common salt (not used in acid poisoning) or rectified spirit (but not used in alcohol, phosphorus, acetic acid, phenol, paraldehyde, formalin, chloroform, chloral hydrate, anesthetic agents, etc.)

2. V2: Liver + gallbladder, spleen, and kidney

500 gm or 1/3rd of liver (whole in infants) 1/2 of the spleen (whole in infants) 1/2 of each kidney (whole in infants)

Saturated solution of common salt (not used in acid poisoning) or rectified spirit (but not used in alcohol, phosphorus, acetic acid, phenol, paraldehyde, formalin, chloroform, chloral hydrate, anesthetic agents, etc.)

3. V3: Blood

100 ml (postmortem) 10 ml (antemortem)

30 mg of potassium oxalate + 10 mg of sodium fluoride/10 ml of blood

4. Urine

100 ml (postmortem) 30–50 ml (antemortem)

3 ml of concentration HCl or 2–3 ml chloroform/100 ml of urine or 100 mg of sodium fluoride per 10 ml of urine

5. Gastric aspirate vomitus

500 ml or whole, if less is available

No preservatives

In food poisoning cases, only the stomach content is preserved without any preservative for detection of toxins and sent to FSL, Mumbai

22

Forensic Toxicology: A Comparative Approach

PRESERVATION OF ADDITIONAL VISCERA/ MATERIAL

Additional viscera or material is preserved in a separate bottle for further analysis in following cases3–9 (Table 2.2): a. In injection deaths: The skin and muscles from injection site is preserved for detection of suspected drugs. A similar part from opposite side is preserved as control sample. b. In burn cases: Skin, hair and clothes are preserved for the detection of petroleum product in cases where required. If clothes are present, then skin/hair is not required for CA as it does not add any advantage. c. In snakebite: Skin from bite site along with blood is preserved for detection of venom. However, it is not detected on TA in almost all cases of poisonous snakebite due to neutralization of toxin. d. In electrocution cases: A part of skin from the site of electrocution injury is preserved for the detection of metallic residues; and part of skin for histopathology. e. In hanging/strangulation cases: Fibers of ligature material are collected by applying transparent cello tape over neck and then wrapped over the plain clean transparent glass slide for comparison. f. In spraying of insecticidal poison: Nasal swabs, hand swabs, clothes, along with lungs and brain. The poison is not detected in routine viscera for TA. g. In cases of criminal abortion: The uterus, cervix, bladder and rectum are preserved. PRESERVATION OF MATERIALS IN SEXUAL OFFENCES

In case of victims, following samples/articles are preserved for Forensic Science Laboratory (FSL): a. Blood for grouping b. Blood for TA c. Urine for TA

d. Seminal stain for grouping and identification e. Nail scrapping for detection of epithelium of assailant f. Pubic hair: Plucked/loose g. Foreign material: Hair/cloth fibers/skin fragment h. Vaginal swabs for detection of seminal fluid (acid phosphatase, etc.) i. Anal/buccal swabs: For detection of semen. j. Clothes—usually the undergarments for seminal stains. In case of accused, following articles are preserved for FSL: a. Blood for grouping b. Blood for TA c. Urine for TA d. Nail scrapping for detection of epithelium of suspect e. Pubic Hair: Plucked/loose f. Foreign material: Hair/cloth fibers/skin fragment g. Clothes Apart from the above materials, the blood is preserved for culture; vaginal swab/smears for detection of spermatozoa; penis/urethral swab/smears for detection of vaginal epithelium. These materials should be sent to department of microbiology or examined by oneself, if facilities are available. MATERIALS PRESERVED IN FIREARM CASE

In firearm case, the body is subjected to radiological examination prior to the autopsy for localization of projectiles (bullet/pellets) and for the track of firearm injuries. Following materials are preserved in firearm cases and sent to FSL for further analysis10 (Table 2.3): 1. Skin from the site of entry and exit. 2. Projectile or related material. 3. Wash sample: Swab moistened with distilled water. 4. Clothes

Preservation of Viscera and Other Materials

23

Table 2.2: Additional viscera/materials and body fluids to be preserved in other specific cases apart from routine viscera for different purposes3–9 Specimen Indication/purpose Quantity Preservative Grouping5,6 2 ml (from cubital vein in AM cases) 2 ml of 5% sodium citrate 1. Blood3–6 2 ml (from heart in PM cases) solution prepared as (5 gm or cotton bandage soaked in sodium citrate + 0.25 ml of 40% blood and dried* formalin + distilled water or two blood stains of 5 cm to make it 100 ml). diameter on sterile cotton cloth* *No Preservative, it is sent in or plucked hair* an envelope after complete or muscle (in saturated saline) air drying. or molar teeth* or bones* TA—for alcohol9, 10 ml (from cubital vein in 1 mg of sodium fluoride + AM cases) 3 mg potassium oxalate/ml7 poisoning cases3, 4 100 ml (from heart in PM cases) Snakebite5 5–10 ml of blood 5% sodium citrate (i.e. 5 gm in distilled water) Volatile poisons or 2–5 ml (from heart in PM cases) A layer of liquid paraffin irrespirable gases added to top of blood to (CO) avoid losses 2. CSF Alcohol As much as possible 10 ml of Na fluoride/ml CSF 3, 7 Alcohol 10 ml 30 mg phenyl mercuric nitrate 3. Urine or thymol per 10 ml of urine7 4 4. Brain a. Dog bite Piece of brain from hippocampus i. Formalin for HP i. For HP cerebral cortex, medulla and ii. 50% glycerine in isotonic ii. For Negri bodies cerebellum saline for Negri bodies b. Alcohol, CO, HCN, 300 gm of brain tissue Saturated solution of anesthetic drugs, common salt opiates, strychnine, barbiturate 5. Spinal cord Strychnine, gelsemium Entire length 6. Lungs Inhaled/volatile poison One

Rectified spirit Saturated solution of common salt 7. Skin with a. Corrosive or injection 5–10 gm of tissue around site Common salt underlying death (insulin, cocaine, or 2 × 2 × 4 cm area with muscle + or rectified spirit tissue morphine, heroin) control skin from opposite side Common salt b. Snakebite5 (skin from 5–10 gm of tissue around bite bite site + control) site + control skin + venous blood 5–10 ml blood 5% sodium citrate From the site of electrocution Common salt c. Electrocution8 injury for detection of metallic residues d. Burns Burnt site for detection of – petroleum products 8. Heart Cardiac poison Complete Saturated solution of common salt 9. Uterus Abortifacient agents in Complete Saturated solution of with its criminal abortion common salt appendages (Contd.)

24

Forensic Toxicology: A Comparative Approach

Table 2.2: Additional viscera/materials and body fluids to be preserved in other specific cases apart from routine viscera (Contd.) Specimen

Indication

Quantity

Preservative

10. Long bones3 Heavy metal poisoning 15 cm of length or 200–300 gm, or bone marrow from sternum/femur 11. Scalp hair3 Heavy metal 15–20 bands (20 gm) for detection of metals Burns 15–20 bands (20 gm) for detection of petroleum products 12. Pubic hair5 Suspected sex violence Plucking or combing in sterile envelope after drying 13. Vaginal or Suspected sex violence In test tube/slide immediately anal swab/ dried in desiccation and kept fluid and separated in TT foreign body5 14. Vomitus3 Poisoning cases 500 ml or whole, if less 15. Stomach Poisoning cases Wash with normal saline— wash 500 ml or whole if less (gastric aspirate)3 16. Nail scraping5 17. Saliva5

18. Soil 19. Clothes

• Suspected sex assault Of all fingers, clipped without • Homicidal/assault damaging underlying tissue to match with accused Grouping Few drops in sterile test tube, or two dried stains of 5 cm diameter on cloth Exhumation articles 20 gm soil as much as possible Grouping—Homicidal Blood stained cloth Sexual offence Undergarment or any stained cloth Poisoning cases Soiled clothes Burns For detection of petroleum products

MATERIALS TO BE PRESERVED FOR DNA FINGERPRINTING (Table 2.4)

In living person (Fig. 2.2) 1. Usually 1.5 ml of blood in 2 plastic tubes containing EDTA. 2. One drop of blood on FTA paper. In dead person 1. Blood if available from heart. 2. Autopsy tissue usually spleen—2 gm. 3. Bone, usually femur/manubrium. 4. In fetus/neonate—blood/femur/sternum. IN UNKNOWN PERSONS FOR IDENTIFICATION

Identification is the main concern of investigation in unknown bodies. It can be

– – – Immediately dried in desiccators Sent in an envelope

– Nil—if wash with normal saline or otherwise with saturated sol of common salt –

– Sent in envelope after drying – Sent in envelope after complete air drying

known from tattoo marks, scar, congenital or acquired peculiarities, clothes and belongings with ornaments. But fingerprints and dental charting is the ideal method for identification. Materials Preserved but not Sent to FSL 1. In dog bite cases4—for detection of Negri bodies in brain, the samples should be sent to Director, Haffkine Institute for Training, Research and Testing, Acharya Donde Marg, Parel, Mumbai–400012. Phone: 022–24160947, 24160961–61, Fax: 022–24161787.

Preservation of Viscera and Other Materials

25

Table 2.3: Materials to be preserved in firearm cases10 Specimen

Quantity

Preservation technique

1. Skin

5–10 cm diameter around site or bearing shot holes

2. Pellets/fragments of bullet + other projectile like wad, etc. 3. Bullet

As many as possible

Keep in two plain white papers stapled to a thick cardboard and tied to another cardboard. Do not put in bottle or in any preservative Dried in air and put in bottle without any preservative

4. Swabs a. Moist with distilled water b. Wet with 5% HNO3 c. Control samples of cotton, HNO3 and distilled water 5. Clothes

Remove with finger or rubber tipped forceps

Dried and wrapped in cotton and put in a suitable container after putting identification mark on the base

From web and fingers of both hands separately in case of alleged firer

Dried in air and put in suitable container

All or bearing shot holes

Dried in air and put in suitable container

Note: X-ray of the body is to be taken prior to the postmortem examination. Injury should be properly described, photograph with a scale attached or sketched and sent along with the articles to FSL for comparison purpose. Table 2.4: Materials/tissue preserved for DNA profile11, 12 (AM = Antemortem, PM = Postmortem) Specimen

Quantity

Preservative

Container

Freezing

Blood liquid

1.5 ml in 2 tubes—AM 2–5 ml in tube—PM 1 drop on FTA paper—AM 5 cm radius on cloth—PM Cotton swabs moistened 3–4 swabs rubbed hard against cheek mucosa or mouth lining scraped with instrument and then smeared onto swab 3–4 swabs

EDTA

Plastic tube

Refrigeration

Air-dried Air-dried

Paper envelope Plastic container

Dry freeze Dry freeze

Air-dried

Plastic container

Dry freeze

Air-dried

Plastic container

Dry freeze

Cotton swab moistened with water or scrapped off if dried 1–20 ml or 1–2 drop

–

Plastic container, paper envelope

Dry freeze

EDTA

Plastic tube

Refrigeration

60–100 ml A few drops 10–20 plucked hair 2 gm (spleen, muscle, etc.) Femur, humerus, sternum All

– – – – – Air dried

Plastic tube Plastic tube Paper envelope Plastic container Paper Paper envelope

Refrigeration Refrigeration Dry freeze Dry freeze – Refrigeration

Blood stain Buccal mucosa

Swabs (oral/ vaginal/rectal) Stain (blood, semen, saliva) Seminal/ vaginal fluid Urine Saliva Hair Autopsy tissue Bone/tooth Bulk clothing

Sometimes, the FSL person (along with kit) is accompanied for collection of blood for DNA profiling. So, if samples are collected and taken to the FSL on same day, then freezing is not required.

26

Forensic Toxicology: A Comparative Approach

2. Histopathological examination of tissue, biochemical and hematological examination, and microbiological examination are not done in FSL, so such materials are not sent to FSL. 3. For bone examination in skeletonized or partially skeletonized body for ascertaining age, sex, etc. the bones should be sent to the Professor and Head, Department of Anatomy4 (of authorized centers) Government Medical Colleges in Maharashtra. 13–15 However, in some states like MP, UP, Chhattisgarh, etc. the bones are examined in the Department of Forensic Medicine usually at medicolegal institute. 4. For entomological examination to determine time since death 16: Live as well as dead eggs, larvae, maggots are collected in two vials. Half to be preserved in ethyl alcohol or formalin (if no other preservative is available) and other half should be kept alive to be reared out without any preservative. Container which contains preserved and living specimen should be properly labelled about date/time of collection, location of remains and the site of collection on the body.17 5. Fingerprints for identification: In Maharashtra, Fingerprinting is under the control of CID of the State (Home department) and not done in FSL. The fingerprints are taken by the police departments in unidentified persons. MODE OF PRESERVATION, PACKING AND DISPATCH OF VISCERA/MATERIALS3,18

1. The collected viscera is preserved in a clean wide mouth standard glass or preferably plastic bottles of ~1 liter capacity. Blood is preserved in 30 ml bottle or plastic capped tubes of 5 ml. Sometimes bottles are supplied by the forensic science laboratory either in cleaned conditioned or it is to be cleaned with sulphuric acid— chromate solution, rinsed with distilled water and dried.

2. V1, V2, V3 should be preserved separately. The additional material should be preserved in separate bottles. 3. However, bone, hair, nails, clothes, etc. are packed in polythene packet or plain paper. But polythene bags or plastic containers are not used in volatile poison (which diffuse through it) and in corrosives poison (which corrode it). Lungs should be preserved in nylon bags for volatile substance. 4. The tissues are open/cut into small pieces before preservation. 5. The preservative is added to each bottle, so as to completely dip the viscera to prevent decomposition. A sample of preservative (100 ml rectified spirit or 25 gm common salt) is separately kept in a bottle and sent for analysis to exclude the possibility of contamination with poison. 6. However, container should not be filled completely and one-third of the container should be kept empty, so as to accommodate the gases liberated due to decomposition of viscera. 7. The bottle is made air tight by putting a lid on it. The lid is also covered with a piece of cloth, and tied with string or tape. 8. The bottle is then properly labeled and the ends of string/tape are sealed. The label contains the PM number; date and time of PM; name, age and sex of deceased; the viscera preserved; the preservative used and signature/seal of medical officer. 9. All sealed bottles containing viscera/ materials are handed over to the concerned police immediately, after taking due receipt. 10. The forwarding viscera form requesting the chemical analyzer to examine the viscera/material, is to be filled by the doctor and sent to FSL along with the viscera. In the forwarding forms/letter to

Preservation of Viscera and Other Materials

27

the chemical analyser, the specimen of seal and copy of label on the material should be included along with the outward number, reference number and description of articles. 11. The police then submit the sealed viscera bottles and sealed viscera form to the concerned chemical analyzer and takes receipt. The copy of PM report is not required to submit the FSL.

collected by the police/investigating officer after autopsy even after due receipt without any information (unless advice to the contrary by the police), then it can be disposed off/ destroyed after 3 months20 considering that it is no longer required.

At some places where viscera box is being provided by chemical analyzer’s office, these sealed bottles are first kept in the viscera box. The box is then closed and locked. Cloth is tied on the lock and sealed. A label is put on the box mentioning the content of the box. The key of the box, viscera form, and a sample seal on a piece of paper corresponding to the seal used on bottles, lock and viscera form are kept in an envelope which is sealed and sent with viscera box. Resealing/relabeling: 18 Sometimes the police bring back the viscera bottle stating that the seal of the bottle is detached or bursting of viscera bottle requesting to transfer the viscera to other bottle or resealing of viscera bottle. Sometimes the label is missing or soiled with the bottle contents, requesting to change the label.18 In such case viscera bottles once sealed should not be resealed or transfer to other bottle, nor the new label be prepared. It is always better to advice the police to prepare a panchnama of the damaged viscera bottle and submit the viscera bottle after proper sealing/labeling to the chemical analyser’s office with a copy a panchnama at the earliest. To avoid soiling/ tampering of the label, it is to be coated with transparent adhesive tape or using plastic coated labels written by permanent marker pen.

b. When informed by the police/investigating officer in writing that the case is closed or viscera are not required for further investigation.

DISPOSAL OF VISCERA19, 20

Viscera/any material or sample collected and preserved for FSL/other department should be handed over to police or investigating officer immediately after completing the autopsy. However, if the viscera is not

It can also be disposed off a. After taking written permission from magistrate or police.

c. When informed by the police/investigating officer in writing about disposal of viscera. Articles/materials which were sent to the FSL for analysis should be removed from the laboratory within 15 days from the date of issue of the report.21 Similarly, the materials which were sent for the histopathological/ anatomical examination are also supposed to remove by the police within 15–30 days from the date of issue of report. INTERPRETATION OF RESULT OF TOXICOLOGICAL ANALYSIS

a. Poison not found in bottles 1 and 2: Poison not detected or it was not a case of poisoning. b. Poison found in bottle 1 and absent in bottle 2: Poison not absorbed or locally acting poison; death is not due to poisoning or locally acting poison or postmortem ingestion of poison. c. Poison found in bottle 2 and absent in bottle 1: Poison is absorbed or poisoning by other routes. d. Poison found in bottles 1 and 2: Poison is absorbed partially. +ve TA Report: When detected poison found in more than fatal level/dose. –ve TA Report: No poison detected or detected in less than fatal level.

28

Forensic Toxicology: A Comparative Approach

REASONS FOR NON-DETECTION OF POISON IN VISCERA22, 23

Sometimes poison may not be detected on chemical analysis due to following reasons: 1. Delay in the examination of viscera and decomposition. 2. Improper preservation. 3. Tampering of preserved viscera. 4. Early disintegration or neutralization of the poison. 5. Denaturation of protein—example snake venom and bacterial toxins. 6. Use of wrong analytical technique. 7. Small amount of sample for analysis. 8. Lack of suitable chemical test for certain poison. 9. Complete metabolism of the poison in the body. 10. Removal/detoxification of poison during treatment. 11. Poison vomited or excreted out completely. 12. Delayed death after poisoning. 13. Some organic poisons such as alkaloids and glucosides, may, by oxidation during life or by putrefaction after death, be split up into other substances which have no characteristic reactions sufficient for their identification. 14. Lastly, due to the unavailability of the standard of specific poisons it will not be detected even if consumed. Example: Vegetables and drug poison. Also, there are various sub-types of insecticidal poison, if the person consumed some particular poison whose standard is not available with FSL, then that particular poison will not be detected/analyzed in spite of the presence of poison in stomach at autopsy. Moreover, if the level/concentration of poison is less than the fatal level, then also the chemical analyser’s report is negative. The detection of poison/drugs in visceral material is also missed particularly when consumed in smaller quantities.24 Court question—about CA report and opinion in poisoning: In most of the admitted poisoning cases and other poisoning cases of vegetable/ animal source, the poison is not detected on toxicological analysis (negative CA report).

In such cases the court will ask the autopsy doctor about the cause of death and the reason for non-detection of poison in the viscera. In an admitted case of poisoning, it is advised not to keep opinion reserved for pending toxicological analysis, where the findings of poisoning were absent due to prolonged admission or gastric lavage or treatment. Rather, the opinion should be given at autopsy as “PM findings are consistent with death due to poisoning” in absence of any other findings suggestive of other cause of death. Even in brought death or spot death of poisoning, the opinion should be given at postmortem examination, if there are findings suggestive of poisoning in the stomach (like kerosene/insecticidal smell with hemorrhagic/eroded mucosa) or other specific findings to particular poisons (like fangs mark in snakebite). In cases of poisoning, the opinion about cause of death is usually possible at autopsy either by way of positive findings of poisoning or by way of exclusion of findings suggestive of other cause of death. The toxicological analysis in such cases reveals only the type of poison, but in many cases it may not reveal any poisons on general and specific chemical testing. Similarly, in food poisoning cases, the toxin will not be detected on TA due to denaturation of toxin. In snakebite cases, the opinion (death due to snakebite) should be given at postmortem examination. Toxicological analysis is almost always negative in such cases due to denaturation of venom. The death is usually due to poisonous snakebite, but can also be possible in non-poisonous snakebite due to fear (neurogenic shock). ALTERNATIVE TO ROUTINE VISCERA IN POISONING CASES

In antemortem cases, stomach wash, blood and urine are preserved in separate bottles for toxicological analysis in case of poisoning. But in postmortem cases, routine viscera from the dead body are preserved in two separate bottles and blood is preserved in third bottle for the detection of poison or intoxicants.

Preservation of Viscera and Other Materials

However, the purpose of detection of poison or intoxicant will be accomplished even if only the gastric content or washing (with normal saline) is sent in place of stomach and intestinal loop with content; blood in place of liver and spleen; and urine in place of kidneys. Moreover, there is no added advantage of sending routine viscera for TA. Thus, the alternative to routine viscera may be: 1st bottle

2nd bottle

Gastric content or gastric washing with normal saline/plain water (100 ml or whole if less is available) Blood from heart—10 ml

3rd bottle

Urine—100 ml

FINGERPRINTING (DACTYLOGRAPHY)

In medicolegal deaths of unknown persons, the fingerprints are taken by the police departments; and analyzed by fingerprint expert. There are 4 types of fingerprints: Loops (65%), Whorls (25%), Arch (7%) and Composite (2–3%) Method of fingerprinting: Fingerprints are taken with the help of printer’s ink on nonglazed papers, after cleaning and drying the fingertips. It may be taken in two ways and are useful when the person is available. 1. Plain method: In this method, the inked finger is brought in contact with the paper and pressed gently. It is clearer and helps to check ridge pattern at a particular place, if the rolled impression is blurred at that place. 2. Rolled method: In this method, one side of the inked fingertip is gently pressed on the paper and rolled onto the other side without lifting finger. Maximum area of the impression is obtained and offer better study of the pattern of ridges, but sometimes may be blurred. FINGERPRINTS FROM THE DEAD BODY

1. A few hours after death, tip of the fingers may get shrivelled in a dead body and may mask the picture. So to avoid this, soak the fingers in alkaline solution25 first and then take the print as mentioned above.

29

2. Fingerprints can be taken from even the highly decomposed bodies, either from the peeled off epidermis of the fingers or from the dermis when epidermis is lost.25 3. Sometimes in dead bodies, the skin and subcutaneous tissues of all the fingertips are dissected out at the request of investigating officer and kept out in weak alkaline solution or normal saline in ten different small clear bottles with markings of initials of finger like RT, RI, RM (Right Thumb, Right Index, Right Middle), etc. respectively. 4. Sometimes in highly decomposed bodies, the skin of hand may be peeled off completely and come out as a ‘gloves’ that may also be preserved completely. In this, fingerprints can be made by inserting the technician finger into the ‘skin glove’, inking the area to be printed and rolling. Plastic fingerprinting are the fingertips impressions left on soft materials like dust, soap or wax. The fingerprints which are not visible as such but made visible are called invisible fingerprinting or latent fingerprinting. Method of development and lifting of fingerprinting:22, 25 The fingerprints which are not visible, are made visible by using various developing agents and the use of these agents depends on the type of surface needed to be searched for fingerprint. a. Physical/powder method: For hard and non-absorbent surface (like glass, porcelain, painted or sun-mica covered surface, metallic articles) but light or dark surface, following powders are used: i. Light/white surface—black powder is used ii. Dark/black surface—grey powder/ aluminum powder is used iii. Multicolored surface—fluorescent type of powder is used iv. Dragon’s blood (a natural powder) may be used for both surfaces. v. Magnetic brush and powders are used to increase the efficiency in development of latent prints. The magnetic brush

30

Forensic Toxicology: A Comparative Approach

marks with magnetic powders are available in many colors like grey, black, red, yellow, etc. Lifting of fingerprinting: Latent fingerprint on the paper or small articles can be preserved as such after development. But when they are on large immovable hard surface, the print can be lifted with transparent cello/adhesive tape of 1.5 or 2 inch width roll after being developed.

Primary classification system of scoring: Scores are allotted for the presence of whorls in different finger of each hand.

b. Chemical methods: For soft absorbent surface (like paper, cardboard, clothes, etc.), iodine vapor, silver nitrate and ninhydrin are used. While committing crimes or in nervous tension there is sweating from body including fingertips through the pores of the skin. When such person holds/touches any object, it produces invisible fingerprint due to moistness. This invisible fingerprint is made visible by different chemicals which react with NaCl, sulphates, phosphates, carbamates, lactic acid, fatty acid, glucose and urea present in the sweating.

The scores are then arranged as follows and one is added for the purpose of calculation.

The following methods (chemicals) are used

Presence of whorls in finger Right thumb (RT)/right index (RI) Right middle (RM)/right ring (RR) Right little (RL)/left thumb (LT) Left index (LI)/left middle (LM) Left ring (LR)/left little (LL)

Scores =

Scoring 16 08 04 02 01

RT + RM + RL + LI + LR + 1 RI + RR + LT + LM + LL + 1

The score of numerator is multiplied with denominator. So, 32 × 32 =1024 scores are possible, if whorls are present in all fingertips. Federal Bureau of Investigation (FBI): USA maintains record of more than two crores fingerprints by systemic maintenance of separate files on the basis of presence of whorls in the finger. In 60% of the world population, there is no whorl in any finger, so according to primary classification, the score is one. On the basis of this scoring, 1024 divisions are made which are called ‘pigeon holes’. Depending on the scoring, final identification of any fingerprint is made by comparison.

i. Iodine method: The iodine fumes reacts with the fatty acids of the print and appears yellowish brown or brownish. ii. Silver nitrate method: It reacts with NaCl to form silver chloride, which is an unstable white substance that darkens, when exposed to light breaking into silver and chlorine that appear reddish brown. iii. Ninhydrin method: It reacts with aminoacid and gives purple reddish brown stains. All the above methods are used for old prints. iv. Osmium tetraoxide method: It is reduced to free osmium that is dark in color in presence of fatty substance.

The technique of DNA fingerprint26 was first developed by Sir Alex Jeffreys of Leicester University, UK in 1984 and developed in India in 1987. It was successfully used in sensational cases like Rajiv Gandhi assassination, famous Tandoori case and recently Madhumita murder case.27

Finder (fingerprint reader): It is a computerized automatic fingerprint reading system which can record each fingerprint data in half seconds. The light reflected from a fingerprint can be measured and converted to digital data which is classified, codified and stored in the computer.

Centers for DNA Fingerprinting Initially it was done only in ‘center for cellular and molecular biology’ (CCMB), Hyderabad. Previously, all the samples were sent to Hyderabad from all regions of India. Now in Maharashtra, new center for DNA fingerprint

DNA FINGERPRINTING

Preservation of Viscera and Other Materials

is established in Regional Forensic Science Laboratories at Mumbai and Nagpur. These centers also provide the kit for collection (Fig. 2.2), preservation and dispatch of samples with prescribed forms.

31

1. Murder 2. Sexual offence 3. Paternity/maternity disputes: Blood from mother, baby and disputed father should be collected. 4. Mixed babies in hospitals 5. Identification of mutilated, dismembered or burnt bodies: The DNA fingerprinting obtained from such remains can be compared with those of close blood relatives of the deceased. 6. Missing person can be identified if his parents or children are available. DIATOM TEST IN DROWNING

Fig. 2.2: Tubes and FTA paper for DNA profile

Materials used in DNA Profiling [Table 2.4] DNA fingerprinting can be done from a wide range of biological specimens in both living and dead person. Biological specimens like blood, bone marrow, semen, hair root sheath, skin and any body tissue, fluid or secretion that contain nucleated cells are used. And cigarette butts, envelops, chewing gum and other articles which can contain saliva are amenable to PCR. Since DNA is very stable, the test can be done on very old stains (aged/ dried stains) or specimens (mutilated/ decomposed bodies). Medicolegal Application Here, the band of DNA is matched with the suspected source or individual.

In 1904, Revenstorf was the first to attempt the use of diatoms in drowning. However, Hoffman discover them in lung fluid in 1896. The basic concept of diatom test is that when a person is drowned in water containing diatoms, the diatoms which enter into the lungs may penetrate the alveolar walls and carried to distant target organs such as brain, kidneys, liver and bone marrow. If diatoms are demonstrated in the tissue of distant organs, then it goes strongly in support of death due to drowning, but there are certain fallacies. But still it is not conclusive in all cases, as it is present in the tissue even when the cause of death is other than drowning. At present the diatom test is used only as an indicative help and not as legal proof of drowning.28 Sample Used for Detection of Diatoms 1. Distant organ tissue like bone marrow (of femur), brain, kidneys: By acid digestion. 2. Test water where victim was drowned: Sedimentation, centrifuge and microscope examination. 3. Control water sample from place of testing: Sedimentation, centrifuge and microscopic examination. Test: For tissue and bone (sternum/femur)28, 29 1. Bone marrow is exposed by cutting a small portion of bone or by crushing it. 2. Small portion (~10 ml) of marrow scooped out into a test tube/crushed tissue—TT.

32

Forensic Toxicology: A Comparative Approach

3. Acid digestion: Add concentration 10 ml conc HNO3 solution in TT × 24–48 hrs. Heat the solution till clear fluid is obtained. 4. Cool and centrifuge at 4000 rpm for 10 min. 5. Examine the sediment under microscope for diatoms. Method to Detect Diatoms from Water (Not 600 mg/100 ml glucose is diagnostic of diabetic.37 Level of >200 mg/ 100 ml in vitreous humor is significant for hyperglycemia38; whereas presence of ketone bodies >5000 μmol/L in vitreous is indicative of diabetic acidosis.39

Preservation of Viscera and Other Materials

2. In renal failure: Well demonstrated level of urea and creatinine in vitreous/ pericardial fluid is indicative of death due to renal failure/uremia.40 High serum or plasma potassium, uric acid, and phosphate concentration usually indicate acute renal failure. 3. Liver failure: Raised serum bilirubin in postmortem sample is indicative of antemortem jaundice. 4. Time since death: It can be estimated from potassium level in vitreous and synovial fluid respectively as follows:35 Death interval (in hour) = 2.71 × potassium level – 20.19 Death interval (in hour) = 2.83 × potassium level – 15.41

There is linear rise of potassium level with increasing time interval after death. 5. Toxic metabolic acidosis in severe poisoning: 41 Measurement of serum/ plasma anion gap can be helpful in differentiating toxic metabolic acidosis (due to poisoning) from that of non-toxic metabolic acidosis. The anion gap is usually calculated as the difference between the sodium concentration and the sum of the chloride and bicarbonate concentrations. (Normally, it is ~10 mmol/L and corresponds to the sum of plasma potassium, calcium and magnesium concentration). This value is little changed in non-toxic acidosis. However, in toxic metabolic a c i d o s i s , the anion gap may exceed 15 mmol/L. Table 2.5: Biochemical conditions in different poisoning41 Conditions

Poisoning

Hypoglycemia

Iron salts, ethanol, paracetamol

Hyperglycemia

Acetylsalicylic acid, salbutamol, theophylline

Hypokalemia

Acetylsalicylic acid, salbutamol, theophylline, barium

Hyperkalemia

Digoxin

Metabolic acidosis Carbon monoxide, ethylene glycol, methanol, paraldehyde or acetylsalicylic. Poisoning with iron, ethanol, paracetamol and theophylline

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b. Plasma Enzymes

1. Time since death: Peak levels of amylase and phosphatase are seen between 36 and 48 hrs after death. It is 48–60 hrs for transaminase and 4th day for lactic acid dehydrogenase.42 2. Fall in serum cholinesterase level is useful indicator in organophosphate or carbamate insecticide poisoning.41 3. High plasma hepatic enzymes are seen in poisoning due to carbon tetrachloride, copper salts, and paracetamol.43 4. Increase gamma glutamyl transferase activity is seen in chronic alcoholism.44 5. Presence of carboxyhemoglobin in blood can be used to assess the severity of CO poisoning and chronic dichloromethane poisoning.41 6. Shock coma and convulsions are often associated with nonspecific increase in plasma or serum activities of enzymes such as LDH, aspartate aminotransferase, and alanine aminotransferase. c. Hemolytic

1. Blood clotting: Prolonged prothrombin time and clotting time is seen in snakebite poisoning (especially viper) and in acute poisoning with hepatotoxic agents, rodenticides containing anticoagulants. 2. Anemia: It is seen in chronic lead, arsenic, copper, mercury and iron poisoning. It is also seen in sickle cell disease with sickle shaped RBCs. 3. Leucocyte count: Leucocytosis is a feature of acute metabolic acidosis resulting from ingestion of methanol and ethylene glycol.41, 43 d. Serological Test It is used in the following circumstances

1. Infection: For detection of antibodies like IgG for old infection and IgM for recent infection. 2. Pregnancy test (hCG in urine): For determination of suspected 1–2 months pregnancy in unmarried suicidal death. 3. Abortion cases up to 7–10 days of abortion for detection of hCG.

34

Forensic Toxicology: A Comparative Approach

4. Food poisoning/gastroenteritis: For detection of toxin. 5. Typhoid: Widal test. 6. Antigen test for malaria. 7. Dengue: NS1 antigen. 8. Viral and antibody test for COVID-19 PRESERVATION OF MATERIAL FOR MICROBIOLOGICAL TEST

Microbiological Investigation It is useful in 1. Food poisoning/gastroenteritis: Swab from small and large intestine for staining and culture/sensitivity of the bacteria. 2. Cholera: Stool sample for hanging drop preparation (for demonstration of motility). 3. Malarial parasites: Peripheral smear, spleen impression for malarial parasite. 4. Sexual offences: Vaginal swab/fluid for detection of sperms and sexually transmitted disease; blood for STD/HIV. 5. Sudden death after trivial injury: Skin tissue from the site of injury/injection should be cultured in Robertson cooked meat media for detection of Clostridium bacilli.45 Blood is preserved for detection of toxins. All samples for microbiological investigation must be collected using sterile instrument and placed in sterile containers. 31 The samples should be sent without delay to the microbiology or pathology department of Government Medical College or Virological Institute if needed. Different samples/swabs are required for bacteriological and virological study. 1. Bacteriological examination: Blood for culture must be obtained in septicemia before organs are disturbed either from heart through 3rd intercostals space or directly from vessels. 31, 46 It is also collected after opening pericardial sac, the anterior surface of right ventricle is seared with heated knife and 10 ml of blood aspirated using sterile needle and syringe. 46 The same technique may be used to remove material from other organs.

The most reliable method of collecting uncontaminated cerebrospinal fluid (CSF) is by spinal or cisternal tap.46 It is collected even after opening subarachnoid space with sterile scalpel, a specimen is taken from a SA space by sterile syringe/ dropper/swabs from which smears and cultures may be made. Urine should be collected using a needle and syringe either through suprapubic puncture before autopsy or by direct puncture to bladder after abdomen is opened.31 For culture of splenic tissue, the surface of the organ is seared with a hot spatula, and the area is punctured with a sterile instrument and pulp is scrapped from which smears and cultures may be made. Samples of gut contents should be taken as soon as possible preferably by tying off about 15 cm length of bowel and removing it, then emptying its contents into sterile container.31 Tissue representing smaller than 6 cm3 is removed aseptically at autopsy and placed in a sealed plastic container and sent immediately or stored in a refrigerator at 4–6oC.46 2. Virological examination: A piece of appropriate tissue or swab is collected under sterile condition and the sample is freezed or preserved in 80% glycerol47 in buffered saline. 3. Feces: 5–10 gm feces is preserved without any preservative for detection of protozoa and helminthes. In cholera cases, hanging drop preparation is prepared from the faecal matter to examine the darting motility of vibrio cholera. 4. Smears of brain cortex and spleen: Stained for malarial parasite. Smears of bone marrow (ribs/sternum): stained for blood dyscrasias. Smears from chancres and mucus patches: Stained or examined fresh by Darkfield for STDs.

Preservation of Viscera and Other Materials

PRESERVATION OF TISSUE FOR ENZYME HISTOCHEMISTRY

It is useful for 1. Determination of age of injury 2. To differentiate between antemortem and postmortem injury. The injured tissue is stained for the presence of enzymes like:48 • Alkaline phosphatase (peak at 4–8 hours), • Acid phosphatase (4 hours), • Aminopeptidase (2 hours), and • ATP-ases and esterase (1 hour). Small pieces of tissues of size ½ × ½ inches from the site of injury with non-injured tissue are excised. The tissue is then cut into two pieces, one part is kept in formalin solution for histology examination and the other part is kept for enzyme histochemistry. For enzyme histochemistry49, the tissue is kept in two ice packs and preserved in a thermos flask containing liquid nitrogen. The sections of 15–16 microns thick are taken in frozen section cryostat. The section is then placed over the slide and fixed with 10% neutral formalin at 4°C for 5 minutes. Then the slide is washed with distilled water and is placed in the jar containing different chemical for specific enzyme in the incubator at 37°C for 1 hour. After treating with various chemicals, the tissue is then examined under microscope for staining of the tissue.

35

2. Injection deaths—part of the tissue at the site of injection is preserved to see local findings of anphylaxis 3. Electrocution/lightening cases 4. Dog bite cases4 5. Poisoning and drug abuse case for degenerative changes in the target organs.50 The tissues are best preserved in 10% formalin or 70% ethanol. For preservation of water soluble elements (such as mucus, glycogen, sodium urate crystals) absolute alcohol is the best preservatives. Tissue size should not be more than 2 × 4 cm and 0.5–1.0 cm thick. Fixing fluid should be at least 25 times the volume of tissue. A typical portion of affected area seen on gross examination should be removed along with adjacent normal tissue. It should be cut into pieces of about 1–2 cm thickness and fixed in 10% formalin or 95% alcohol. The tissue should be preserved in a jar, labeled and sealed as soon as possible. It should be dispatched to the department of pathology directly or usually through police along with histopathology form (Fig. 2.3).

PRESERVATION OF TISSUE FOR HISTOPATHOLOGICAL (HP) EXAMINATION

In some of the medicolegal cases, the tissue from the suspected pathology of the organ is preserved for histopathological examination. The microscopic examination of tissue not only helps to confirm the pathology on gross examination but also in a few other medicolegal cases while framing the cause of death. The Tissue for HP Examination It is preserved in 1. Pathological conditions

Fig. 2.3: Tissues preserved for histopathology

PRESERVATION FOR MUSEUM SPECIMEN

There is lot of disagreement whether it is legal to keep the organs removed during medicolegal autopsies for museum purpose. There are no

36

Forensic Toxicology: A Comparative Approach

valid guidelines in this regard as it is a medicolegal case and consent of the relatives is not taken for medicolegal postmortem. But, in surgical practice, if the ill organ with certain pathology or injury is removed, then it is either retained by the department for museum purpose or for histopathology or disposed of by incineration. In routine medicolegal practice, after completion of the autopsy, the particular organs having gross pathology or injury may be retained by forensic department for museum purpose, so that it will be useful for academic/teaching purpose for the students. There are two methods51 of preservation for museum specimen. Method I: Kaiserling’s Method (1897) 1. Firstly the tissue/organ is rinsed in cold water. Then placed in Kaiserling-1 solution Potassium nitrate Potassium acetate Formalin Distilled water

10 gm 30 gm 200 ml 1000 ml

• For 2–14 days depending upon the size of tissue (1 × 6 × 6 cm tissue kept for 2 days). 2. Washed in running water for 20 minutes. 3. Then placed in Kaiserling-2 solution (comprising 80% ethyl alcohol). • For 10 mins–1 hr or until original color restored. 4. Again washed in running water and then placed in vacuum desiccators filled with Kaiserling-3 solution: Potassium acetate Glycerine Formalin (40%) DW

100 gm 200 ml 50 cc 1000 ml

and subject to a negative pressure of at least 50 mm Hg for 1 hr or more. 5. Mount the specimen in airtight museum jar filled with freshly filled Kaiserling-3 solution.

Method II: Dithionite method for restoration of natural colour Tissue fixed for 3–4 days in Kaiserling solution or formalin can be recolorized. 1. Fixed or fresh tissue are again fixed in following solution for 3–4 days. Formalin Common salt Distilled water

1000 ml 300 gm 5000 ml

2. They are thoroughly washed in tap-water for 1–3 hours. 3. Next treated with following solution for 2–3 days at least thrice. Formalin Distilled water Sodium dithionite (Na2S2O4) Potassium carbonate Pyridine

1000 ml 5000 ml 100 gm 30 gm 20 ml

4. Change the fluid or treat the tissue with above solution at least thrice. 5. They are finally mounted in glass or museum jar and filled with fresh solution. IMPORTANT QUESTIONS

1. Describe mode of preservation, packing and dispatch of viscera for toxicological analysis. Add a note of negative chemical analyser report. 2. How will you preserve routine viscera for toxicological/chemical analysis in a case of poisoning? What are the indications of viscera preservation and their interpretation of the result? 3. Write about disposal of viscera not taken by the police after postmortem cases. 4. Describe the reason for non-detection of poison in viscera. How will you frame opinion as to the cause of death in such cases? 5. Describe the method for collection, preservation and dispatch of samples for DNA fingerprinting. 6. Discuss about removal of material after autopsy but are not required to be forwarded to FSL for further examination.

Preservation of Viscera and Other Materials

7. Write about preservation of tissue for histopathological examination. 8. Describe the utility for preservation of material/postmortem sample for biochemical and microbiological investigation at autopsy. 9. Describe methods of preservation of organ for museum purpose. SPECIFIC LEARNING OBJECTIVES

After reading this chapter, the reader should be able to: • Delineate the guidelines for preservation of routine/additional viscera for toxicological analysis • Enumerate the different indications of preservation of viscera in poisoning cases • Recognize the different materials preserved in sexual offences, firearms, DNA profiling, identification, etc • Understand the procedure of packing and dispatch of viscera/materials • Explain the method of disposal of viscera • Recognize the alternative to routine viscera in poisoning cases • Enlist reasons for non-detection of poison in the viscera/material • Enumerate different materials for preservation in biochemical and serological estimation for various medicolegal cases • Enumerate different materials for preservation in microbiological and histopathological examination in various medicolegal cases • Summarize the steps involved in preservation of viscera for museum specimen References 1. S.G’s Circular Memo No. PML46/4868/11850/B dated 9th May 1968. In: Maharashtra Civil Medical Code. Chapter 13: Forensic Science Laboratories, Para 13.5 (A)(i) . Vol 1, 1977: 106–22. 2. Home Department Circular No. PRO 2360/ 57359/IX dated 12th JAN 1962. In: Maharashtra Civil Medical Code. Chapter 13: Forensic Science Laboratories, Para 13.5 (A)(i). Vol 1, 1977: 106–22.

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3. SG’s Memorandum No. PLM-4863/6224 Dated 22nd March 1963; and SG’s Circular Memo No PML/18/467/14809/B dated 7th July 1969. In: Maharashtra Civil Medical Code. Chapter 13- Forensic Science Laboratories, Para 13.5 (A)(ii). Vol 1, 1977: 106–22. 4. Forensic Science Laboratories. In: Maharashtra Civil Medical Code. Chapter 13, Para 13.5 (A)(iii). Vol 1, 1977: 106–22. 5. Forensic Science Laboratories. In: Maharashtra Civil Medical Code. Chapter 13, Para 13.5 (B). Vol 1, 1977: 106–22. 6. Govt Letter UDPH and HD No HD/FSL 3064/ 29239/4263G Dated 9 Dec 1965. In: Maharashtra Civil Medical Code. Forensic Science Laboratories. Chapter 13, Para 13.5 (B). Vol 1, 1977: 106–22. 7. Bardale R. Inebriant poison. In: Principles of Forensic Medicine and Toxicology. 1st edn, Jaypee Brothers Medical Publishers (P) Ltd: New Delhi. 2011: 511–27. 8. Forensic Science Laboratories. In: Maharashtra Civil Medical Code. Chapter 13, Para 13.5 (A)(iv). Vol 1, 1977: 106–22. 9. Forensic Science Laboratories. In: Maharashtra Civil Medical Code. Chapter 13, Para 13.5 (D). Vol 1, 1977: 106–22. 10. Forensic Science Laboratories. In: Maharashtra Civil Medical Code. Chapter 13, Para 13.5 (C). Vol 1, 1977: 106–22. 11. Kagne RN, Ambade VN, Pathak AG. DNA fingerprinting: Collection, preservation and dispatch of biological sample. Souvenir of Formedicon 2004, XIIth Annual Conference of Medicolegal Association of Maharashtra, 2004, 39–42. 12. Knight B. DNA profiling. In: Forensic Pathology. 2nd edn, Arnold: London. 1996: 597–8. 13. Government Resolution No FSL 1966/6724– XXII, dated 12th May 1967, Government of Maharashtra, regarding examination of medicolegal cases by Anatomy. 14. Government Resolution No. CRA-697 dated 6 Feb 1998, Home Department, Government of Maharashtra, regarding authorization of centers for bone examination. 15. Ambade HV, Kasote AP, Fulpatil MP, Meshram MM. Medicolegal Cases for Bone Examination: 11-Year Retrospective Study. Journal of Indian Academy of Forensic Medicine. 2018; 40(1):102–6. DOI: 10.5958/0974-0848.2018.00017.9 16. Rosilawati R, Baharudin O, Syamsa RA, Lee HL, Nazni WA. Effects of preservatives and killing

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Forensic Toxicology: A Comparative Approach methods on morphological features of a forensic fly, Chrysomya megacephala (Fabricius, 1794) larva. Tropical Biomedicine. 2014; 31(4): 785–91. Lord WD, Rodriguez WC. Forensic Entomology: The use of Insects in the investigation of Homicide and Untimely death. Winter 1989: 41–8. SG Circular Memo PML/18/467/14809/H dated 7th July, 1969. In: Maharashtra Civil Medical Code. Chapter 13: Forensic Science Laboratories, Para 13.5 (A) (iii), 1977: 106–22. Para No 123 and 145 (2) of Police Manual, Home Department, Maharashtra. In: Maharashtra Civil Medical Code. Chapter 13: Forensic Science Laboratories, Para 13.5 (A) (iii), 1977: 106–22. SG Endorsement No 1662/1072/D, dated 17 Sept 1962 on IGP’s Letter to the SG. In: Maharashtra Civil Medical Code. Chapter 13: Forensic Science Laboratories, Para 13.A(iv), 1977: 106–22. Forensic Science Laboratories. In: Maharashtra Civil Medical Code. Chapter 13, Para 13.6, Vol 1, 1977: 106–22. Mathiharan K, Patnaik AK. Chapter 1 Section II. Toxicology. In: Modi’s textbook of medical jurisprudence and toxicology, 23rd edition, Lexis Nexis: New Delhi. 2006: 26. Bardale R. Toxicology Medicolegal consideration. In: Principles of Forensic Medicine and Toxicology. 1st edn, Jaypee Brothers Medical Publishers (P) Ltd: New Delhi. 2011: 432–6. Non-detection of poison on CA SG’s Circular No PML 4863/6224/B dated 2nd June 1967. In: Maharashtra Civil Medical Code. Chapter 13: Forensic Science Laboratories, Para 13.5 (A) (iv), 1977: 106–22. Nandy A. Identification of an individual. In: Principles of Forensic Medicine. 2nd edn, Reprint. New Central Book Agency (P) Ltd: Calcutta. 2004: 93–7: Fingerprints. Jeffreys AJ, Brookfield JFY, Semenoff R. Positive identification of an immigration test case using human DNA fingerprints. Nature. 1985; 317: 818–9. DNA profiling in Justice delivery system. Central Forensic Science Laboratory, Kolkata. Ministry of Home Affairs, Government of India. 2007. Assessed on: wbja.nic.in › wbja_adm › files › dna profiling cfl Knight B. Diatoms and diagnosis of drowning. In: Forensic Pathology. 2nd edn, Arnold: London. 1996: 404–6.

29. Nandy A. Violent asphyxial deaths. In: Principles of Forensic Medicine. 2nd edn, Reprint. New Central Book Agency (P) Ltd: Calcutta. 2004: 331–3; Diatoms 30. Karmakar RN. Forensic Medicine and Toxicology: Theory, oral and practical. Academic Publishers: Kolkota. 5th edn, 2015: 68–72. For urine preservatives. 31. Sheaff MT, Hopster DJ. Post Mortem Technique Handbook. 2nd edn. Springer-Verlag London Ltd: USA. 2005: 326–31. 32. Tumram NK, Ambade VN, Dongre AP. Thanotochemistry: study of vitreous humour potassium. Alexandria J of Medicine, 2014, 50:365–8. 33. Tumram NK, Ambade VN, Dongre AP. Thanotochemistry: study of synovial fluid potassium. Alexandria J of Medicine, 2014, 50:369–72. 34. Dalbir Singh and Rajendra Prasad. Relationship between the postmortem intervals and the pericardial enzyme activities in subjects of Chandigarh zone of India—A preliminary study. J Indian Acad Forensic Med. 2009; 31(1): 30–6. 35. Tumram NK, Bardale RV, Dongre AP. Postmortem analysis of synovial fluid and vitreous humor for determination of death interval. Forensic Sci Int. 2011; 204: 186–90. 36. Sagar Vidya, Berry V, Chaudhary RJ. Diagnostic value of serum enzymes—A review on laboratory investigations. Internat. J Life Sci and Pharma Res. 2015; 5(4): 8–12. 37. Arieff AI, Carroll HJ. Hyperosmolar nonketotic coma with hyperglycemia: abnormalities of lipid and carbohydrate metabolism. Metabolism 1971;20:529–38. 38. Coe JI. Postmortem chemistry update: Emphasis on forensic application. Am J Forensic Med Pathol. 1993; 14(2):91–117. 39. Pounder DJ, Stevenson RJ, Taylor KK. Alcoholic ketoacidosis at autopsy. J Forensic Sci. 1998 Jul; 43(4):812–6. 40. Palmiere C, Mangin P. Urea nitrogen, creatinine, and uric acid levels in postmortem serum, vitreous humor, and pericardial fluid. Int J Leg Med. 2015 Mar;129(2):301–5. 41. Flanagan RJ, Braithwaite RA, Brown SS, Widdop B, de Wolff FA. General Laboratory findings in clinical toxicology. In: Basic Analytical Toxicology. WHO in collaboration with UNEP and International Labour Organisation: Geneva. 1995: 13–7. 42. Nandy A. Death and postmortem changes. In: Principles of Forensic Medicine. 2nd edn, Reprint. New Central Book Agency (P) Ltd: Calcutta. 2004: 168–71.

Preservation of Viscera and Other Materials 43. Pillay VV. Modern Medical Toxicology. 4th edn, Jaypee Brothers Medical Publishers (P) Ltd: New Delhi. 2013: 581–2. 44. Teschke R. Gamma-glutamyltransferase and other markers of alcoholism. In: Seitz HK, Kommerell B (eds). Alcohol related diseases in gastroenterology. Springer, Berlin Heidelberg, New York. 1985: 48–64. 45. Ananthanarayan R, Paniker CKJ. Textbook of Microbiology. 6th edn. (reprint). Hyderabad: Orient Longman Private Ltd. 2002: 229. 46. Ludwig Jurgen. Special Methods. In: Current methods of autopsy practices. 1st edn. WB Saunders Company: Canada. 1979: 207–16.

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47. Johnson FB. Transport of viral specimens. Clinical Microbio Reviews. 1990. P. 120–31. 48. Knight B. The pathology of wounds: Histochemical changes in injured tissues. In: Forensic Pathology. 2nd edn, Arnold: London. 1996: 165–6. 49. Drury RAB, Wallington EA. Enzyme Histochemistry. In: Carleton’s Histological Technique. 5th edn, Oxford University Press: Oxford, New York. 1980:298–322. 50. Patel F. Ancillary Autopsy–Forensic histopathology and toxicology. Med. Sci and law, 1995; 35: 25–30. 51. Drury RAB, Wallington EA. Museum and injection techniques. In: Carleton’s Histological Technique. 5th edn, Oxford University Press: Oxford, New York. 1980:474–88.

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Forensic Science 3 Laboratory and Analytical Methods Including Psychoanalysis Forensic science laboratories (FSLs) are the laboratories working under Union Government or State Government for the examination of physical evidences sent either by doctors after clinical examination/ postmortem examination or recovered from the scene of crime in different criminal and civil cases. Thus, it helps to link the victim/accused to the crime or incident. As the person (chemical analyser) working in FSL are using different analytical methods for the analysis of different physical evidences to link the suspect to the scene, they should be rightly called “Forensic Scientist” instead of “Forensic Expert”. Almost all the states have their FSL to carry out analysis of physical evidences. In Maharashtra1, there are four FSLs at Mumbai (1958), Pune (1979), Aurangabad (1981) and Nagpur (1968). Two more laboratories have been started at Nashik (2004) and Amravati (2009).

FSL is having following sections for different purposes:2

the help of chromatography and spectrophotometer. 6. Prohibition and excise section: It helps to detect blood alcohol concentration in consumption/possession cases under Bombay Prohibition Act. It also examines ganja, charas, bhang, opium, etc. 7. Document analysis: For examination of handwriting, typewriting, forged documents and currencies. 8. Photography section: Evidences from various exhibits and materials.

1. Toxicology section: For toxicological analysis of viscera and other body fluids/ materials or suspicious articles in different poisoning cases. 2. Biology/serology section: For blood group estimation and identification of body fluids, hair and plant material in murder, assault, rape and disputed paternity case. It also helps in food poisoning and skull superimposition cases. 3. Physics (including photography) section: For examination of trace materials in murder, theft, vehicle accident, etc. by spectrographic, X-ray, thermoanalytical, photomicrographic method. 4. Ballistic and explosive section: For microscopic examination and chemical analysis of firearms and explosive material. 5. General analytical and instrumentation (GAI): It deals with chemical analysis of petroleum products, explosive material, dyes, chemicals, drugs of abuse in murder, arson, theft, cheating, etc. with

It also has following sections with the advancement of crime: 1. Tape authentication and speaker identification (TASI): It helps to determine whether any audio/video tape is edited, tampered or altered. Every human being has a unique voice like fingerprint; thus helps to identify the speaker and record certain characteristics in his/her voice by using advanced computerised method. 2. DNA fingerprinting section: For identification of individual. It is a costly method but has a broad application in forensic 40

Forensic Science Laboratory and Analytical Methods Including Psychoanalysis

investigation like paternity dispute, murder, rape, etc. 3. Cyber forensic: It helps to extract important data from computer, mobiles, SIM cards, debit/credit cards. So it helps not only to crack cyber crimes but also in murder, accidents, etc. from location of the mobiles. 4. Polygraphy section: For lie detection. 5. Narcoanalysis and brain mapping: For extracting truth. 6. Mobile evidence collection unit: For collecting different evidences from the crime spot directly under the supervision of police. PHYSICAL EVIDENCE

It includes weapons, knives, blunt instruments, firearms, bullets, cartridge cases, wads, blood, seminal stains, saliva, epithelium, hair, poisons, fingerprints and foot/shoe prints, broken pieces of glass, vehicles paint, oil, grease, soil, clothes, documents, and cigarette butts, etc. It is useful to prove the crime and also connects with the suspect. Examples 1. In Poisoning In poisoning, stomach wash, blood, urine, feces and vomitus apart from routine viscera at autopsy are sent for chemical analysis. In food poison, only the stomach contents are preserved without any preservative and should be sent to chemical analyzer for detection of toxin. a. Toxicological analysis of viscera/body fluids to know nature of poison. b. Analysis of food/utensils, bottle/clothes, etc.—provides corroborative evidence in food poisoning. 2. In Assault and Murder In homicide, examination of certain object/ material from the body or scene helps to detect crime and for identification of accused/ victim. a. Blood grouping from blood stains on victim, hair in victim’s hand, saliva on cigarette butts for identity of assailant.

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b. Clothes examination for identification. c. Examination of weapon/object to detect crime. 3. In Burn Deaths In this, the clothes and hair are sent to chemical analysis for detection of petroleum product (like petrol, kerosene). However, examination of metallic objects, teeth and bones also helps in identification of the charred body. 4. In Sexual Offences In this, the examination of different samples is collected for chemical analysis. It helps to know whether the offence has been committed and to identify the accused. a. Examination of vaginal fluid, blood/ seminal stains—to check whether crime has been committed. b. Examination of hair, epithelium, blood grouping for identity of accused. c. Examination of clothes—site of offence, identity of accused. 5. In Vehicular Accident

a. Blood for CA for alcohol detection (especially driver) b. Blood grouping for identification/matching c. Tyre marks to compare with the type of offending vehicle. d. Grease, mud, blood, tissues, glass pieces, hair, paint, etc. on vehicle to indicate offending vehicle. e. Examination of clothes/site to identify accused. 6. In Firearm Injuries

a. Examination of projectile (bullet/pellet) to know the nature and type of firearm. b. Examination of markings on bullet—to know which gun was used in firing by comparison method. 7. In Explosion and Blast Examination of the material/soil from the core of blast for detection of explosives material.

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Forensic Toxicology: A Comparative Approach

8. In Hanging/Strangulation For matching of ligature material used in hanging and strangulation. a. The fibers of ligature on the neck are taken by applying transparent cellotape over the mark and then stuck onto a clean glass slide. It is then compared with the fibers of ligature material used. b. Also the epithelial tissue adherent over the ligature should be compared with the tissue of the victim. 9. Identification Identification is the main concern in unknown, decomposed and skeletonized bodies. It can be known from fingerprints, footprints, clothes, tattoo marks, scar, or any acquired or congenital malformation. This can also be possible by DNA fingerprinting, fingerprints, superimposition technique and reconstruction of face. 10. Disputed Paternity/Identity The cases can be settled by blood grouping and DNA fingerprinting. DNA matching can be done by collecting amniotic fluid/ chorionic membrane or by collecting blood from the umbilical cord and matching with suspected biological father. Recently, it can also be done by just collecting maternal blood for fetal cells.

11. Drug Addiction/Drug Trafficking/Drug Reaction This can be known from detection of drugs in tissues and vials/specimen along with blood for CA. ANALYTICAL METHODS USED IN TOXICOLOGY

In any particular case of poison, it is important either to know the nature/type of poison (qualitative analysis) or to know both type and concentration of poison in the body (quantitative analysis). The preservation of proper sample is the most important step in any toxicological analysis. The result of any analytical method depends on the amount and purity of the extract obtained from different biological materials (like viscera, stomach wash/vomit, urine, blood and tissue sample). The method for isolation/extraction of the poison not only depends on type of poison (pesticide, volatile, drugs, alkaloids, metallic, etc.) but also on the type of biological material3. After the isolation/extraction of the poison from biological material kept for toxicological analysis, screening/color test for different poisons can be done before any analytical method for quantitative estimation. 1. QUALITATIVE ANALYSIS I. Screening/Color Tests (Table 3.1)

Table 3.1: Screening/chemical test used for detection of different poisons Names of test 1. Chemical test: Acid4–6

Procedure

Result

Indicates

BaCl2 + H2SO4  BaSO4 H2SO4 + FeSO4 + HNO3 AgNO3 + HCl  AgCl BaCl2 + TM*

White precipitates Junction: Brown ring White curdy ppt White barium oxalate crystals

H2SO4 HNO3 HCl Oxalic acid5

Ferric chloride 1 ml of 10% ferric chloride + 2 ml TM (urine) test7

Blue color substance/ Phenol, persistent purple color phenothiazines, phenylbutazone, or salicylates

Ferric chloride 2 ml of TM + few drops of FeCl2 test6

Red color  disappear Acetic acid on HCl

2. Chemical Hydroxides + AgNO3 test: Alkalies8 Carbonates + HCl *TM: Test material

Yellow precipitates White precipitates

Alkalies (Contd...)

Forensic Science Laboratory and Analytical Methods Including Psychoanalysis

43

Table 3.1: Screening/chemical test used for detection of different poisons (Contd...) Names of test 3. Metallic poison: Marsh’s test9

Reinsch test6,9

Gutzeit test10

Procedure

Result

TM is placed in a hydrogen generator  Arsine is formed which comes out through the narrow mouth of a generator and burns with a blue or greenish flame and gives garlicky smell.

If the porcelain plate is Arsenic plate at the top of the flame, then greyish metallic arsenic is deposited, which is soluble in hypochlorite solution

20 ml TM (stomach content) in conical flask + 10 ml HCl + strip of copper—heated × 1 hr in a boiling water bath inside a fume cupboard. Copper is removed and examined.

• Bluish black

TM in large TT + Pure Zn+ 3 drops of Filter turns yellow dil HCl + Pot iodide. A plug of absorbent cotton wool is inserted in Filter turns brown or the upper part of TT and mouth of black TT is covered with a filter paper moistened with concentrated solution of silver nitrate.

Ammonia test TM in TT + few drop of NH4OH 6

• Silvery deposit • Black deposit

Deep blue precipitate

Indicates

Mercury Arsenic (dull black) or bismuth (shiny black) Antimony Arsenic Antimony

Copper

HCl acid test

1 ml TM in TT + 1 ml dil HCl

White ppt, dissolves on Lead boiling and reappears on cooling

Ammonium sulphide test11

Ammonium suphide + TM containing ferric/ferrous salt 

Black precipitate, soluble in dil. HCl

Iron

Deep blue precipitates

Ferrous or ferric iron

Yellow color

p-nitrophenol derivative like parathion, chlorthion OC

Ferro-cyanide 50 ml of filtered stomach content + 100 ml HCl + 50 ml test12 potassium ferrocyanide solution. 4. Agricultural A fraction of extracted residue in poisons: 1 ml ethanol in micro crucible + 1 ml OP: KOH test6 KOH (10%) and heated OC: Sulfuric acid test6

Test extracted residue + Toluene + 2 drops of fuming sulfuric acid reagent

Red color

Carbamate: HCl test6

Mixture of extracted residue + 5 drops ethanol applied over Whatman paper No 1 and dried, exposed to vapor of HCl

Steel blue color spot on Carbamate paper

Silver nitrate test13

Patient is asked to breath in and out through a piece of filter paper impregnated with 0.1N AgNO3 sol × 5–10 min

Filter paper turns black • Aluminium/zinc due to presence of phosphide phosphine in breath • Hydrogen sulphide

TT: Test tube

(Contd...)

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Forensic Toxicology: A Comparative Approach

Table 3.1: Screening/chemical test used for detection of different poisons (Contd...) Names of test

Procedure

Result

Indicates

Dithionate test:12

1 ml of test sample + 0.5 ml of aqueous ammonium hydroxide (2 mol/L). Mix for 5 sec + 20 mg of solid sodium dithionate.

Blue to blue black color Yellow-green color

Paraquat

5. Veg Irritant: Marquis test6

Dried residue of extract in TT + 1 drop of Marquis reagent

Brown color Pink color

Ergot Abrus

NaOH test6

2 ml of extract in alcohol + 2 ml NaOH

Brownish red ring

Croton tiglium

Sulfuric acid test6

2 ml of residue of extract + 1 ml H2SO4

Pink/purple color

Calotropis gigantea

6. Somniferous poison: Marquis test6

One drop of mixture (3 ml conc H2SO4 + 3 drops formalin) on a blotting paper soaked with TM (gastric fluid)

Purple color that gradually turns blue

Opium/morphine

7. Inebriant poison: Dichromate test12

Filter paper soaked with potassium dichromate is placed at the mouth of test tube containing test material (urine). Heat × 1 min.

Color of filter paper changes from orange to green.

Alcohol

Phosphoric acid-sodium bisulfite— chromotropic acid test6

0.5 ml distillate in TT + 0.2 ml Violet color phosphoric acid + 0.2 ml KMnO4. Add sol of sod bisulfite till brownish color persist. 1 drop phosphoric acid + 1 drop sod bisulfite + 5 ml chromotropic acid

Chromotropic 0.5 ml distillate in TT + 5 ml chromotropin acid. Heated on acid test6 hot water bath at 60°C × 30 min and cooled

Formaldehyde

Red color Yellow color

Atropine Hyoscyamine

Purple red color

Cannabis

Whitish/yellowish ppt, soluble in potassium cyanide

Bromides

TT-A: Sample + NaOH + Pyridine TT-B: Putrified water + NaOH + Pyridine TT–C: Trichloroacetic acid +NaOH + Pyridine  Heat in boiling water bath × 2 m

A. Red/purple color B. No color C. Red/purple color

Chloral hydrate, chloroform, TC Ethylene

2 drops extract in acetic acid in porcelain dish + pinch of Mn dioxide. Lines drawn with rod dipped in MnO2 and H2SO4

Play of color from blue-violet-purple-red and finally yellow

Strychnine

Residue of extract in TT + small amount of FBB reagent + 1 ml chloroform  shake

9. C. Depressant: Br + AgNO3– Silver nitrate test14 Fujiwara test (1 ml each in all three test tubes)12

10. Spinal: Manganese dioxide test6

Methyl alcohol

Violet color

8. Deleriant: 2 ml of 2% mercuric chloride in 50% Gerrard’s test6 alcohol added to extract. Fast blue B test6

Diquat

(Contd...)

Forensic Science Laboratory and Analytical Methods Including Psychoanalysis

45

Table 3.1: Screening/chemical test used for detection of different poisons (Contd...) Names of test

Procedure

Result

Indicates

11. Cardiac poison: LeeJones test:15

5 ml gastric fluid + few crystals of FeSO4 + 5 drops of 20% NaOH—boil and cool. Then add 8–10 drops of 10% HCl

Greenish blue color Purple color

Cyanide Salicylates

Test for digitalis6

TM + conc H2SO4

Green color Yellow to brick red Red color

Digitoxin Digitalin Digitonin

Keller test6

Ether extracts in viscera + 1 ml GAA. Put over mixture (100 part of conc H2SO4 + 1 part FeSO4)

Blue color on GAA Violet color on H2SO4 layer

Cerbera thevetia

Mayer’s reagent test6

Dried residue acidified with AA + 2 drops of reagent

White/yellowish ppt

Nicotine

Palet’s reaction test6

1 ml extract in acetic acid in dish. Heated and dried. Drops of Phosphoric acid + sod molybdate is added. Heated

Violet color vapor appears

Aconitine

Test for CO poisoning16

1 ml of test blood + 10 ml water

If >20% sat of CO turns pink

CO

12. Food poisoning: 5 ml adulterated mustard oil + 5 ml Nitric acid test6 Nitric acid  shake the test tube

Orange yellow color

Argemone

Melzer’s test17 Spores of mushroom are stained with 1 drop of Melzer’s reagent and viewed under microscope.

Spores turn to bluish black color

Amanita phalloides of toxic mushrooms

Tensilon test18 In sudden paralysis, 10 mg edrophonium is given IV.

• If dramatic recovery • If no recovery

Myasthenia gravis Botulism

Melxner test19

Squeeze a drop of juice from the fresh tissue onto a piece of pulp paper or mash it on a paper and encircle it with a pencil and dry it. Put few drops of conc HCl.

Blue color within a few minutes

Amatoxin present in mushrooms

Drugs: DilleKoppanyl test6

TM extract on spot plate + 4 drops cobaltous acetate + 4 drops isopropylamine sol (5%)

Reddish-purple

Barbiturates

Marquis reagent test6

1 ml of TM extract in TT + few drops of marquis reagent

Yellow or orange color Benzodiazepines

Trinder’s test12

2 ml urine + 100 ml Trinder’s reagent × mix for 5 sec

Violet/purple color If turns darkens

Salicylates Negative test

Trinder’s reagent: 40 g mercuric chloride in 850 ml water + 120 ml of aqueous HCl mixed with 40 g hydrated ferric nitrate diluted to 1 L with warm water. If the test sample is other than urine like stomach contents, etc. then it should first be hydrolyse by heating with 0.5 mol/L HCl in a boiling water bath × 2 min, and neutralise with 0.5 mol/L sodium hydroxide FPN test:12

1 ml of test sample (urine/stomach content) + 1 ml FPN reagent

Color from pink, red violet to blue Green/blue color

Phenothiazines. Tricyclics (Contd...)

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Forensic Toxicology: A Comparative Approach

Table 3.1: Screening/chemical test used for detection of different poisons (Contd...) Names of test

Procedure

Result

Indicates

FPN Reagent: 5 ml Ferric chloride + 45 ml perchloric acid + 50 ml HNO3 O-Cresol test:12

Forrest test:12

0.5 ml test sample + 0.5 ml conc HCl  heat in boiling water bath × 10 min and cool. Then add 1 ml aqueous o-cresol solution (1 gm/L) + 0.2 ml test mixture + 2 ml ammonium hydroxide (4 mol/L)— mix × 5 seconds

Blue or blackish color

Paracetamol or Phenacetin

0.5 ml test sample + 1 ml forrest reagent × 5 seconds

Yellow green color deepening to blue

Imipramine and related compound

Forrest reagent: 25 ml pot. Dichromate + 25 ml H2SO4 + 25 ml perchloric acid + 25 ml HNO3

II. Thin Layer Chromatography (TLC) TLC is a simple, and widely used, inexpensive qualitative technique, which involves movement by capillary action of a liquid phase through a thin, uniform layer of stationary phase (usually silica gel) held on a rigid support. 2. QUANTITATIVE ANALYSIS

If the positive result of any suspected poison is obtained from the qualitative analysis (chemical/ bed side test), then its estimation is carried out by quantitative analysis (Table 3.2). This can be done with the help of the following methods:

1. Ultraviolet spectrophotometry (UVS) 2. Gas chromatography (GC) 3. High performance liquid chromatography (HPLC) and high performance thin layer chromatography (HPTLC) 4. Mass spectrometry (MS) 5. Radioimmunoassay (RIA) 6. Enzyme-mediated immunoassay technique (EMIT) 7. Atomic absorption spectrophotometry 8. Neutron activation analysis (NAA)

Table 3.2: Comparison between GC, HPLC and HPTLC Comparison points

GC

HPLC

HPTLC

1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14.

Solid Gaseous – Volatile Invisible Closed Tubular column 1 sample Full High temperature Essential Medium Medium 5–25

Liquid Liquid – Non-volatile Invisible Closed Tubular 1 sample Full High pressure Essential High Very high 5–25

Solid Liquid Gas Non-volatile Visible Open Planar (plate) up to 20 × 5 stepwise Room T and P Not essential Low Low up to 100

Stationary phase Mobile phase Conditioning phase Samples should be Sample System Separating medium Analyzed at a time Automation Operation required Sample clean up Maintenance Running cost Samples/shift

Forensic Science Laboratory and Analytical Methods Including Psychoanalysis

ANALYTICAL TECHNIQUES

1. Chromatography It is a technique to separate mixture of substances, based on differences in the relative affinities of the substances for two different media—one, a moving fluid (the mobile phase) and other, a porous solid/gel/liquid, coated on a solid support (the stationary phase or sorbent). The speed at which each substance is carried along by the mobile phase depends upon its solubility and on its affinity for the sorbent. It is used to detect poisons and chemicals. a. Thin Layer Chromatography (TLC) In TLC, the stationary phase is a thin layer of absorbent, e.g. silica gel coated on a rectangular plate and the mobile phase is a solvent mixture. The sample is applied to a spot on the plate which is made to stand in solvent. As the solvent rises through the absorbent, the components of the sample are carried along at different rates and can be visualized as a row of spots, after the plate is dried and stained or viewed under UV light. b. Paper Chromatography It is similar to TLC. But the stationary phase is a sheet of special grade filter paper. c. Column Chromatography It is a type of chromatography using a sorbent packed in a column. The sample dissolved in a solvent, is poured on the top. Some components are retained in the column bound to the sorbent. They are then washed out in suitable solvents. d. Gas Chromatography (GC) It is a more sophisticated system of quantitative analysis. It offers a way of simultaneously separating, identifying, and measuring drugs and other organic poisons. It is a type of chromatography in which the sample dissolved in a solvent is vaporized and carried by an inert gas through a column packed with a sorbent to any of the several types of detectors. Each component of sample, separated from others by passage through

47

the column, produces a separate peak in the detector output, which is graphed by a chart recorder. The sorbent may be an inert porous solid (gas-solid chromatography) or a nonvolatile liquid coated on a solid support (gasliquid chromatography). e. High Performance Liquid Chromatography (HPLC) This is similar to GC, except that it is not restricted only to volatile compounds. It can be used to separate and analyze complex mixtures as well. f. High Performance Thin Layer Chromatography (HPTLC) This is the fastest of all chromatography methods. It can analyze about 100 samples of 5–10 different types per shift. It is a visual technique where the chromatogram (separated sample after chromatography) is visible. In this, the stationary phase is solid, whereas in HPLC, the stationary phase is liquid. TLC is the method of choice for impurity analysis of pharmacopeias. It is not useful for the detection of unknown poison. Rather it is helpful to find out the impurities in known pharmacological samples.

2. Electrophoresis (Electrochromatography) It is a technique used to separate mixture of ionic solutes in an applied electric field. The speed at which the solutes are separated depends on the difference in their rate of migration. The original method in which the movement of the solvent is unrestricted is termed moving boundary electrophoresis, because all the particles of a single species move at the same rate, maintaining a sharp boundary. This method involve a support medium such as paper, cellulose acetate, agarose gel, starch gel or polyacrylamide gel, which prevents convective motion of the solvent; this is called zone electrophoresis. The electrically charged protein components move on the phase plate. The plate is then treated with coloring agent which causes appearance of visible characteristic bands specific for a particular protein.

48

Forensic Toxicology: A Comparative Approach

3. Spectroscopy Every substance absorbs light of specific wavelength thus producing dark bands in specific zones. With the help of spectroscope, the light of specific wavelength is propagated through the medium/solution and then analyzed. Thus, it helps in the identification of various forms of hemoglobin. 4. Spectrophotometer It estimates the quantity of coloring matter in the solution by the quantity of light absorbed after passing through the solution by means of spectrophotometer. a. Colorimeter Using filters, the light of specific wavelength is allowed to pass through the test substance, and the rays absorbed are detected. b. UV/lR Spectrophotometry This technique is based on the principle that many drugs when in solution will absorb ultraviolet (UV)/infrared (IR) radiation. The degree of absorption depends on the chemical structure of the drug, its concentration in the solution, and the wavelength of the rays. The amount of UV/IR radiation that passes through the solution is measured by the photocell. This technique is ideal to quantitative blood levels of paracetamol and salicylates, as well as urine levels of phenothiazines. A major disadvantage of UV spectrophotometry is the possibility of interference in multiple drug overdoses. c. Mass Spectrometry (MS) The testing material in minute amount is placed in high vacuum chamber, and is bombarded with electrons. The molecules of the material, lose electrons, get positively charged, and break into fragments, which get separated according to their mass in an electromagnetic field. The same is recorded as lines in a graph. This is usually combined with gas chromatography (GS-MS), and is considered to be the best technique for quantitative analysis of

wide variety of chemicals, but its expense greatly restricts its use. d. Emission Spectrophotometry Every element on being excited emits light spectrum which can be separated and recorded by photography. e. Atomic Absorption Spectrophotometry (AAS) The element is vaporized and through this radiations from a light source are passed. This displaces the electrons of the atoms resulting in emission of energy which is recorded graphically. This is the best method for detecting inorganic elements (arsenic, lead, mercury, thallium, etc.). However, it requires a large sample of blood for accurate analysis. The organic matrix is combusted and the metal forms a cloud of atoms, which absorbs a fraction of the radiation in proportion to the concentration of metal in the sample.

5. Neutron Activation Analysis (NAA) It is based on the principle that many substances become radioactive when exposed to bombardment by neutrons. It can be used for the estimation of any of the 90 naturally occurring elements from antimony to zinc. This is highly sophisticated and expensive method of detection of a variety of inorganic elements to analyze very small quantity of matter. It is carried out in firearm cases to detect firearm residue. ACRO-Reaction Test It is done in electric current death for detection of metallic residue (pearls) at the site of entry. 6. Radioimmunoassay (RIA) It is slow and expensive method of detecting drugs in the blood, but is highly accurate. It involves mixing known quantities of drugspecific antibody with known amount of radioactively labeled drug that allows analysis of the precipitate with a gamma counter. It is excellent for the detection of drugs in extremely low blood concentration (cannabis, LSD, paraquat, digoxin, etc.).

Forensic Science Laboratory and Analytical Methods Including Psychoanalysis

7. Enzyme-mediated Immunoassay Technique (EMIT) It is a fast, expensive method with good accuracy. It works on the principle that the amount of drug present is proportional to the inhibition of an enzyme-substrate reaction. A known quantity of a drug is labeled by chemical attachment to an enzyme. Drugspecific antibodies added to the specimen bind the drug–enzyme complex, thereby reducing enzyme activity. Free drug in the specimen competes with enzyme labeled drug and limits the antibody-induced enzyme inactivation. Enzyme activity correlates with the drug concentration in the specimen as measured by absorbance change resulting from the enzyme catalytic action on a substrate. EMIT is preferred over other RIA methods because of its simplicity and speed in providing information on toxic drug concentrations. There are two main disadvantages 1. Negative result does not exclude the ingestion of a drug that may be present in undetectable quantities. 2. Antibodies cross-reactions can produce false positive results. 8 Microscope a. Comparison Microscope (Color Contrast Microscope) It is an instrument which permits simultaneously viewing of parts of images of two separate specimens involving two microscopes bridged together with a comparison eyepiece or one microscope, with two body tubes and lens systems. b. Darkfield Microscope (Ultra Microscope) It is a microscope with a central stop in the condenser, permitting diversion of light rays and illumination of the object, from the sides, so that details appear light against a dark background. c. Electron Microscope It is the microscope in which an electron beam, instead of light, forms an image for

49

viewing, allowing much greater magnification and resolution. The image may be viewed on fluorescent screen or may be photographed. d. Fluorescence Microscope It is the microscope, used for the examination of specimens stained with fluorochromes, e.g. fluorescein labeled antibody which fluoresces in UV light. e. Polarizing Microscope It is a microscope, equipped with polarizer, analyzer and means for measurement of the alteration of the polarized light by the specimen. f. Scanning Microscope/Electron Microscope It is a microscope, in which a beam of electrons scans over a specimen, point by point and builds up an image on the fluorescent screen of a cathode ray tube. g. X-ray Microscope It is a microscope in which a beam of X-ray is used instead of light, the image usually being produced on film.

9. Psychoanalytical Test (DDT Test) With the increase in crime incidence, the police interrogation techniques play a vital role in extracting the truth from the suspect. The scientific methods have been developed for extracting confession. Following scientific tests also known as deception detection tests20 (DDT) are used as police interrogation tools: a. Lie detector or the polygraph test b. P300 or the brain mapping test c. Narcoanalysis or the truth serum test d. The brain electrical oscillation signature (BEOS) The polygraph test was among the first scientific tests to be used by the interrogators. These psychoanalytical tests are also used to interpret the behavior of the criminal (or the suspect) and corroborate the investigating officers’ observations.

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Forensic Toxicology: A Comparative Approach

a. Polygraph or Lie Detector Test It records various physiological responses represented by mechanical or electrical impulses, such as respiratory movements, pulse wave, blood pressure and skin sensitivity21 (psychogalvanic reflex). Such phenomenon reflects emotional reactions which are of use in detecting deception. Polygraph test is conducted in three phases: 21 A pretest interview, actual test (chart recording) and post-test interrogation/ diagnosis. The pre-test interrogation consists of a medical/personnel history, and educational background of the examinee. After that the examiner (a clinical or criminal psychologist) prepares a set of test questions (not more than 12 questions to avoid any discomfort to the examinee)21 depending upon the relevant information about the case provided by the investigating officer, and reviews them with the examinee in the same sequence as they will be put during the test. After explaining about the instrument and attaching the different components of the instrument to the body, the actual test is started by asking from the set of test questions. All questions must be asked in moderate tone without any inflexion of the voice. The procedure is repeated after allowing time for the subject to relax. Post-test interrogation is done for the purpose of obtaining further information.21 Polygraph is based on the theory that when a person tells a lie, there is a fear that his lie would be detected. It results in stimulation of symphathetic nervous system resulting in physiological and behavioral changes. These changes can be recorded in the polygraph. However, these changes may also be triggered by anxiety, fear, confusion, hypoglycemia, psychosis, depression, etc.20 Hence, the reliability has been repeatedly questioned. b. P300 or the Brain Mapping Test or Brain Fingerprinting This test was developed and patented in 1995 by neurologist Dr. Lawrence A. Farwell, Director and Chief Scientist “Brain-wave Science”, IOWA.22 Dr. Farwell has published

that a Memory and Encoding Related Multifaceted Electroencephalographic Response (MERMER) is initiated in the accused when his brain recognizes noteworthy information pertaining to the crime.22 These stimuli are called the target stimuli. In this method, called the “brain-wave fingerprinting” the accused is first interviewed and interrogated to find out whether he is concealing any information. Then sensors are attached to the subject’s head and the person is seated before a computer monitor. He is then shown certain images or made to hear certain sounds. The sensors monitor electrical activity in the brain and register P300 waves, which are generated only, if the subject has connection with the stimulus, i.e. picture or sound. It measures the changes in the electrical field potentials produced by the sum of neuronal activity in the brain by means of sensors.20 The changes directly related to specific perceptual or cognitive events.23 Thus, brain generates a unique brain-wave pattern when a person encounters a familiar stimulus.24 The subject is not asked any questions. In a nutshell, brain fingerprinting test matches information stored in the brain with information from the crime scene. Studies have shown that an innocent suspect’s brain would not have stored or recorded certain information, which an actual perpetrator’s brain would have stored. The Forensic Science Laboratory in Bangalore is the first center in India, which conducts the brain-mapping or brain-fingerprinting test. In the USA, the FBI has been making use of “Brain-mapping technique” to convict criminals. c. Narcoanalysis or Truth Serum Test It is one of the scientific tools of interrogation for extracting confessions/truth after giving certain anesthetic and sedative drugs by putting a subject into a hypnotic state. This lowers a subject’s inhibition in the hope that the subject will more freely share information and feelings.

Forensic Science Laboratory and Analytical Methods Including Psychoanalysis

Historical background The term narcoanalysis was coined by Horseley. Narcoanalysis first reached the mainstream in 1922, when Robert House, a Texas obstetrician used the drug scopolamine on two prisoners.22 Narcoanalysis was rather unheard in India till recent past. It was first used in 2002 in the Godhra carnage probe. It was again in news in the Telgi stamp paper case in December 2003 at a government hospital in Bangalore. Later on, it was done in number of criminal cases like Nithari serial killing case, Talwar murder case, etc. Principle and theory This is based on the principle that at a point close to unconsciousness the person cannot resist questions and also not be able to speak lie, which he had been to conceal his crime. The underlying theory is that a person is able to lie by using his imagination. In the narcoanalysis test, the subject’s imagination is neutralized by making him semiconscious. The subject is not in a position to speak up on his own but can answer specific and simple questions. In this state, it becomes difficult for him to lie and his answers would be restricted to facts, he is already aware of. His answers are spontaneous as a semiconscious person is unable to manipulate his answers. Drugs25 and dose

1. Scopolamine hydrobromide 2. Sodium amytal or sodium pentothal 3. Sodium seconal The narcoanalysis test is conducted by mixing 3 g of sodium pentothal or sodium amytal dissolved in 3000 ml of distilled water.22 Depending on the person’s sex, age, health and physical condition, this mixture is administered intravenously along with 10% of dextrose over a period of 3 hours with the help of an anesthetist.22 The rate of administration is controlled to drive the accused slowly into a hypnotic trance, resulting in a lack of inhibition.

51

The team In India, the narcoanalysis test is done by a team26 comprising of an anesthesiologist, a psychiatrist, a clinical/forensic psychologist, an audio-videographer, and supporting nursing staff. The forensic psychologist will prepare the report about the revelations, which will be accompanied by a compact disc of audio-video recordings. Procedure It is completed in four stages25 i. Pre-test interview: Giving all the information to the subject about the test and consent is taken. ii. Pre-narcotic state: Drug is being given to maintain pre-narcotic state throughout the interview. iii. Semi-narcotic state: When the subject appears to be flushed with slurred speech and nystagmus, the forensic expert/ psychiatrist facilitates the interview, the subject is allowed to sleep off and allow to wake up. iv. Post-test interview: In this, the subject got relax after the interview. The complete procedure of interrogation is recorded in audio-visual format and the report is prepared by the experts, which helps in the process of collecting evidence. This procedure is conducted in government hospitals after a court order is issued instructing the doctors or hospital authorities to conduct the test. Personal consent of the subject is also required. Reliability Although inhibitions are generally reduced, people under the influence of truth serums are still able to lie and even tend to fantasize. Different aspects of narcoanalysis test

1. It helps a lot in crime prevention and detection. 2. It also helps in getting clinching evidence and is an effective and non-hazardous method of inducing hypnosis.

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Forensic Toxicology: A Comparative Approach

3. If a criminal was put under narcoanalysis then he would reveal about the crime committed, where he had hidden the weapons used in committing the crime and why did he do it? 4. This would help in getting the motive for the crime and collect other evidence needed for prosecution. 5. Narcoanalysis is also considered by many to be definitely better than third degree treatment to extract truth from an accused. But on the other hand, it has following drawbacks: 1. It required highly qualified physician for administration of drug and its analysis. 2. Dose depends on individual physique and mental attitude and will power, so difficult to determine correct dose. 3. Wrong overdose may lead the individual into coma or even death. 4. If the subject is an abuser of other intoxicants/narcotics, the test could be false due to cross tolerance. d. Brain Electrical Oscillation Signature (BEOS) An Indian Scientist, Champadi Raman Mukundan as developed a technology called Brain Electrical Oscillation Signature test.27 The concept behind this electroencephalography (EEG) technology is that, it is able to show like as functional MRI, activated areas of the cortex which are then localized and the implications are determined. It deals with the experiential knowledge of the person. The Visual and Auditory Stimulus Programming (VASP) system allows recording and compilation of the probe like in different scenarios, marking events, etc. as well as creating video presentation for priming the subject. The probes are presented in a predefined manner by the VASP computer. They are sequentially interlinked and are designed after extensive interviews with the investigation officers and the suspects. Noncontroversial information is used as ‘control probes’. The ‘neutral probes’ are used for

baseline correction. When the experiential knowledge is consistently present for relevant sequence of event, the test findings are said to be forensically significant. Legal Aspect on DDTs The interrogation of the accused by the police plays an important role in collecting evidence. But, if the culprit remains silent and does not answer any questions of the investigating agencies, then to what extent the investigating agencies can force the accused to extract truth. Moreover, any confession made to the police is not considered valid in the court of law; and police torture is not acceptable to extract truth as per human rights and ethics. So, in such circumstances can investigation agencies use DDT to extract information about crime.20 There are many who support that such tests often help the investigation agencies to extract truth. But others reject it as a clear violation to constitutional provisions. These psychoanalytical methods as a tool of police interrogation also raises serious concerns related to the professional ethics of medical personnel involved in the administration of these techniques and violation of human rights of an individual. 28 In this regards, National Human Rights Commission had published Guidelines in 2000 for the Administration of Polygraph test.20 In a landmark judgment 29 , the Madras High Court ordered that investigating agency is required to complete investigation within a reasonable time. If not completed, the benefit is given to the accused. If the accused fails to cooperate with the investigation process during custodial interrogation, then scientific investigation methods may have to be carried out to find the truth.29 On May 5, 2010 the Supreme Court in India28 in Smt. Selvi and other vs. State of Karnataka declared brain mapping, lie detector tests and narcoanalysis to be unconstitutional, violating Article 20 (3) of Fundamental Rights. These techniques cannot be conducted forcefully on any individual and requires consent for the same. When they are conducted with consent, the material so

Forensic Science Laboratory and Analytical Methods Including Psychoanalysis

obtained is regarded as evidence during trial of cases according to Section 27 of the Evidence Act.20 IMPORTANT QUESTIONS

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4. Qualitative analysis test for identifying organic functional groups of homologous series of molecules identification—for anions identifying negative ions hydroxide (alkalis) identification. http://www.docbrown.info/page13/ ChemicalTests/ChemicalTestsa.htm#Sulphate.

1. Describe different divisions of forensic science laboratories of the state and its function.

5. Reddy KSN, Murthy OP. The Essential of Forensic Medicine and Toxicology. 32nd edn, Om Sai Graphics: Hyderabad. 2013: 503–9.

2. Describe different screening test for metallic poison or agricultural poison. Add a note on ‘non-detection of poison’ in the viscera sent after postmortem examination.

6. Jaiswal AK, Millo T. Screening/spot/color test for different poisons. In: Handbook of Forensic Analytical Toxicology. 1st edn, Jaypee Brothers Medical Publishers (P) Ltd: New Delhi. 2014: 81– 174.

3. Describe different scientific methods of interrogation for extracting confession from the criminals by police. 4. Describe different psychoanalytical method (Deception Detection Test) of investigation for extracting truth from the culprits. Discuss legal point of view in such investigation. SPECIFIC LEARNING OBJECTIVES

After reading this chapter, the reader should be able to: • Understand the purpose of different sections of FSL • Enlist various chemical tests for the detection of different poisons • Enumerated different analytical techniques • Describe different psychoanalytical tests (Deception Detection Tests) like polygraph, narcoanalysis, brain mapping. • Understand legal aspects of DDTs. References 1. Forensic Science Laboratories. In: Maharashtra Civil Medical Code. Chapter 13, Para 13.1, Vol 1, 1977: 106–22. 2. Forensic Science Laboratories. In: Maharashtra Civil Medical Code. Chapter 13, Para 13.4,. Vol 1, 1977: 106–22. 3. Jaiswal AK, Millo T. Extraction/isolation and Clean-up methods. In: Handbook of Forensic Analytical Toxicology. 1st edn, Jaypee Brothers Medical Publishers (P) Ltd: New Delhi. 2014: 45–79.

7. Pillay VV. Textbook of Forensic Medicine and Toxicology. Paras Medical Publisher: Hyderabad, 17th edn, 2016: 497–520. 8. Nandy A. Corrosive Agents. In: Principles of Forensic Medicine. 2nd edn, Reprint. New Central Book Agency (P) Ltd: Calcutta. 2004: 455–66. (For alkalies) 9. Nandy A. Metallic chemical irritant. In: Principles of Forensic Medicine. 2nd edn, Reprint. New Central Book Agency (P) Ltd: Calcutta. 2004: 475–90. (For metallic poison) 10. Sanger CR, Black OF. The quantitative determination of arsenic by the Gutzeit method. Proceedings of the American Academy of Arts and Sciences. 1907; 43(8): 297–324. 11. Dikshit PC. Textbook of Forensic Medicine and Toxicology. 2nd edn, PEEPEE Publisher and Distributors (P) Ltd., New Delhi. 2014: 482–500. (For iron). 12. Analytical Toxicology: Flanagan RJ, Braithwaite RA, Brown SS, Widdop B, de Wolff FA. Qualitative tests for poison. In: Basic analytical toxicology. WHO in collaboration with UNEP and International Labour Organisation: Geneva. 1995: 34–49. 13. Bardale R. Principles of Forensic Medicine and Toxicology. 1st edn, Jaypee Brothers Medical Publishers (P) Ltd: New Delhi. 2011: 490–9. 14. Reddy KSN, Murthy OP. The Essential of Forensic Medicine and Toxicology. 32nd edn, Om Sai Graphics: Hyderabad. 2013: 557–9. 15. Lee-Jones M, Bennett MA, Sherwell JM. Cyanide self poisoning. Brit Med J. 1970; 4; 780–1. 16. Pillay VV. Textbook of Forensic Medicine and Toxicology. Paras Medical Publisher: Hyderabad, 17th edn, 2016: 640–54.

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17. Leonard LM. Melzer’s Lugol’s or Iodine for identification of white-spored Agaricales. Mcllvainea, Spring 2006. 16(1): 42–51.

24.

18. Pascuzzi, Robert M. The edrophonium test. Seminars in Neurology.2003; 23 (1): 83–8. 19. Melxner. The Melxner test for Amatoxins in Mushrooms. Mycena News. 1979; 29(9): 74. In: Clinical toxicology. 1980;16(3):401–2. 20. Math SB. Supreme Court judgement on polygraph, narcoanalysis and brain mapping: boon or bane. Indian J Med Res. 2011; 134(1): 4–7. 21. Camps FE. The Polygraph (Lie Detector). Gradwohl’s Legal Medicine. 2nd edn, John Wright and Sons Ltd: Bristol. 1968: 545–7. 22. Nagaraja MR. 3rd degree torture by doctor and police: SOS e Voice for justice _ e- news weekly. 24/10/2015. Vol 11 (43). https://sites.google. com/site/sosevoiceforjustice/3rd-degreetorture-by-doctors-police. Assessed on 08/10/ 2019. 23. Lefebvre CD, Marchand Y, Smith SM, Connolly JF. Use of event-related brain potentials (ERPs)

25.

26.

27.

28.

29.

to assess eyewitness accuracy and deception. Int J Psychophysiol. 2009;73:218–25. Dickson K, McMahon M. Will the law come running? The potential role of “brain fingerprinting” in crime investigation and adjudication in Australia. J Law Med. 2005;13:204–22. Sharma BR. Scientific Criminal Investigations. 1st Edn. 2006, University Law Publication: New Delhi. pp. 60–1. Barnwal AK, Sole AN Development of narco Analysis Test as Investigation Technique In The Criminal Justice System: An Indian Perspective IOSR Journal Of Humanities And Social Science (IOSR-JHSS). 2016; 21(7): 97–102. Rose NS. Reading the Human Brain: How the Mind Became Legible. Body and Society. 2016; 22(2), 1–36. Selvi, Ors vs State of Karnataka. Judgment on 5 May 2010. (Criminal Appeal No. 1267 of 2004). Assessed on 10/10/2019. http://supremecourtofi ndia.nic.in/ Dinesh Dalmia vs. State of Tamil Nadu, Crl. R.C. No. 259 of 2006. Madras High Court.

4 Corrosives Corrosives refer to any chemical (strong acids or alkalies) that dissolves or destroys the structure of an object. However, caustic (sometimes used as a synonym) refers only to the strong bases, particularly alkalies and not to the acids. Thus, corrosives are the substance which corrode and damage the tissue on contact causing chemical burns. In dilute form, they act as an irritant. Strong acids react violently with water and generate heat and fire.1 So, never pour water in it and when diluting, always add it slowly to the water. Sulfuric acid, nitric acid and hydrochloric acid are the examples of inorganic strong acid; and oxalic, carbolic and acetic acids are examples of organic strong acid. Hydroxide and carbonates of sodium, potassium, calcium and ammonium are the examples of strong alkalies. Actions 1. Destruction and corrosion by burning of tissues on contact with acids. 2. Coagulation of tissue protein 3. Fixation of tissues 4. Extraction of water from the tissues (hygroscopic) and liberate heat2, 3 5. Convert hemoglobin into acid hematin4 6. Carbonization of organic matter

SULPHURIC ACID Synonyms

NITRIC ACID Synonyms

HYDROCHLORIC ACID Synonyms

Oil of vitriol, battery acid.

Red spirit of nitre, aqua fortis

Muriatic acid, spirit of salts

Chemically: H2SO4

Chemically: HNO3

Chemically: HCl

Source Industries, commercial, laboratories

Source Source Industries, commercial, laboratories Industries, commercial, laboratories, household

Uses • Wet batteries • Diatom test • Fertilizer manufacturing • Ore processing • Oil refining, drain cleaner

Uses • Used by goldsmith, • In explosives: Picric acid, nitrocellulose • In fertilizer

Uses • Cleaning of ceramic surface • Preparation of chlorine • Treatment of achlorhydria • In hemoglobin estimation • In leather processing

Properties1, 2 1. Colorless 2. Odorless

Properties6, 7 1. Colorless/yellowish tinge 2. Pungent7/choking odor8

Properties9, 10 1. Colorless 2. Pungent odor (Contd...)

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Forensic Toxicology: A Comparative Approach

3. Non-fuming 3. Fuming 3. Non-fuming 4. Burning sour taste 4. Burning sour taste 4. Burning sour taste 5. Carbonises organic matter5 5. Xanthoproteic reaction8: Nitric It chars tissue and blackened acid reacts with organic proteins organic matter to cause nitration of phenyl group 6. Oily, heavy and hygroscopic and forms picric acid to cause yellow discoloration 6. Powerful oxidizing agent dissolves all metals except gold and platinum Clothes: Burns instantly, black

Clothes: Yellow staining4

Clothes: Whitish or grey stain

Action: Locally corrosives

Action: Locally corrosives

Action: Locally corrosives

Fatal dose: 5–10 ml

Fatal dose: 10–15 ml

Fatal dose: 15–20 ml

Fatal period: 12–24 hours

Fatal period: 12–24 hours

Fatal period: 12–24 hours

Clinical features 1. Intense burning pain, difficulty in speech and deglutition, dyspnea (edema of larynx), vomiting, thirst, excessive salivation with blood and mucous, hoarseness of voice (inflammation of epiglottis and larynx), abdominal pain, constipation,5, 11 suppression of urine and dehydration followed by shock • The vomitus is strongly acidic mixed with altered blood (brown or black due to hematin), mucous and mucous membranes 2. There is erosion of mucosa from lips to stomach. There is also erosion of skin along line of trickling of acid from the mouth due to constant drooling of saliva or acid spillage while swallowing.12 Yellowish color

Grey color12, 13

3. Teeth:4 Chalky white

Yellowish

Not significant

4. Perforation: Common

Less common

Uncommon

Erosion: Blackish color

5. On inhalation: Irritation of the eyes, lacrimation, photophobia, burning sensation in the throat, cough and dyspnea.1,7 Immediate death can result due to suffocation. Causes of death: Shock, laryngeal spasm, perforation peritonitis, septicemia, malnutrition Treatment 1. Emetics and gastric lavage are contraindicated (perforation of stomach). 2. Drinking of plenty of plain water or wall scrapping or toothpaste or non-flatulent antacids11. 3. Weak solution of non-carbonated alkalies like CaO, MgO (4TSF in a pint of water or milk) and lime water, aluminum hydroxide 4. Demulcent drinks like milk, egg albumin, vegetable oil, ghee, butter, starch, etc. 5. Supportive treatment for pain, dehydration and shock. 6. Tracheostomy and artificial respiration is required for laryngeal edema; laparotomy and surgical repair for perforation. 7. Wash the affected part with water and soap or sodium/potassium carbonate; followed by application of thick paste of magnesium oxide or sodium carbonate.5 Postmortem findings: It depends upon the concentration of corrosive and the period of survival. A. In early deaths Gross corrosion of skin and mucous membrane of mouth, tongue and lips with discoloration Stomach: Wall—soft, swollen, Mucous membrane (MM)—desquamated, ulcerated, hemorrhagic with discoloration Contents—acidic, altered blood, mucous, epithelium shreds (Contd...)

Corrosives Corrosion color:3 Blackish

Yellowish

Gastric perforation and peritonitis: Very common Common

57 Brownish Uncommon

B. In late deaths: Signs of repair or infection may be present Medicolegal aspect: 1. Suicide: Mostly used for suicide 2. Homicide: Rarely used for homicide, especially on children. It is also used for acid bath murder (hydrochloric acid/sulphuric acid).13, 14 3. Accidental poisoning: May occur in laboratory or goldsmith shop, mistaken with liquid paraffin or castor oil. It also occurs due to inhalation of acid fumes/vapor in factories. 4. Abortifacient: Sometimes used to procure criminal abortion. 5. Vitriolage: They are commonly used for throwing on other person. 6. Punishment for adultery/infidelity by putting acids in the vagina of a woman.4, 11 7. For forgery purpose: Hydrochloric acid is used to erase writings.15 Material preserved: Routine viscera in rectified spirit Stained scrapping— no preservative Clothes: No preservatives

Material preserved: Material preserved: Routine viscera in rectified spirit Routine viscera in rectified spirit Stained scrapping—no preservative Stained scrapping—no preservatives Clothes: No preservatives Clothes: No preservatives

Diagnosis 1. Chemical test:4, 5, 16 BaCl2 + H2SO4  BaSO4 (white ppt.)

H 2 SO 4 + FeSO 4 + HNO 3 brown ring AgNO3 + HCl  AgCl at the junction of two fluids (white curdy ppt.)

2. Blue litmus paper test:3,16 Acid turns blue litmus paper red

Fig. 4.1: H2SO4

Fig. 4.2: HNO3

Fig. 4.3: HCl

VITRIOLAGE Definition: It is throwing of any corrosive substance (usually acids) on other person out of jealousy or to take revenge with the intension to cause injury, disfigurement or death. Since sulphuric acid (oil of vitriol) is commonly used, hence the name Vitriolage. Acid filled in old electric bulbs are usually used for vitriolage. Substances used: Sulphuric acid, nitric acid, hydrochloric acid, sodium/potassium hydroxide, and marking nut juice.

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Forensic Toxicology: A Comparative Approach

Features of vitriolage 1. Chemical burns: In the form of disfigurement of face or body with burn injury. It is characterized by: a. Discoloration and staining of clothes and body b. Absence of vesicles/blisters c. Trickling marks of an acid d. No red line of demarcation 2. Eye: Blindness, corneal destruction or conjunctival edema Cause of death: Neurogenic shock or septicemia Treatment 1. Wash the affected part with plenty of water and soap or sodium/potassium carbonate. 2. Apply thick paste of magnesium oxide or sodium bicarbonate.5 3. Eyes are irrigated with water or dilute solution of sodium bicarbonate.5 4. Treat like a case of burns, using antibiotic and steroid ointments and eyedrops. Medicolegal aspect Grievous injury due to disfigurement of any part of the body by throwing of an acid.17 It is also due to permanent privation of hearing and vision of either side as per Section 320 IPC.18

OXALIC ACID

CARBOLIC ACID

ACETIC ACID

Synonyms: Acid of sugars

Phenol, phenic acid, phenyl alcohol

Glacial acetic acid (100% conc.), vinegar (4–5%)19

Chemically: C2H2O4

Chemically: C6H5OH

Chemically: CH3COOH

Source Industries, commercial, laboratories, household (metal cleaning, stain remover)11, vegetables—onion, spinach, cabbage, radish, carrot, beet

Source Industries, commercial, laboratories, household (disinfectants), it is a coal tar derivative

Source Industries, commercial, laboratories, household (vinegar)

Uses • To erase writing and signature for forgery purpose5 • For ink/rust stain removal • For calicoprinting4 • For metal/glass cleaning • In bleaches (esp. pulp wood)

Uses Uses • Used as disinfectant/antiseptic • Used in food • Accepted as snake repellant • Medicinal use in superficial ear • In cosmetics/sunscreen, hair infection, jelly fish sting and dyes, skin lightening bladder irrigation preparations

Properties20

Properties21

Properties22

1. Colorless, transparent, shining crystals (resemble MgSO4 and ZnSO4) 2. Odorless/irritating smell 3. Burning sour taste 4. Hygroscopic 5. Vaporizes on heating and sublimates on cooling11

1. White small needle like crystals, on exposure to air, it becomes light pink liquid 2. Sweetish acrid odor 3. Burning sweet taste 4. Hygroscopic 5. Crude carbolic is phenyl, which is dark brown in color

1. Colorless liquid, when freezes becomes crystalline solid 2. Vinegar, pungent smell 3. Burning sour taste 4. Volatile liquid

Action 1. Locally: Corrosives

Action Action 1. Locally: Corrosion, necrosis and 1. Locally: Corrosives

Corrosives

59

2. Systemic: It causes hypocalcemia Gangrene of the local area. 2. Respiratory distress by utililization of serum 2. Systemic: CNS—first stimulate calcium to form oxalate. and then depresses 3. Nephrotoxicity—oxaluria 3. Nephrotoxicity—carboluria

Fig. 4.4: Oxalic acid

Fig. 4.5: Phenol

Fig. 4.6: Acetic acid

Fatal dose: 10–15 gm Fatal period: 2–12 hrs

Fatal dose: 10–20 gm Fatal period: 2–12 hrs

Fatal dose: Uncertain Fatal period: Uncertain

Clinical features Locally: There is corrosion of mucosa of mouth, tongue and lips—whitish or yellowish. Skin—Whitish or yellowish discoloration12,20

Clinical features: (Carbolism) Locally: There is corrosion of mucosa of mouth, tongue and lips—grayish white. Skin—reddened, necrosis and gangrene.

Clinical features Locally: There is corrosion of mucosa of mouth, tongue and lips. Skin—no corrosion, redness, blisters22

1. GIT: Intense burning pain, difficulty in speech and deglutition, dyspnea (edema of larynx), vomiting, abdominal pain, thirst, excessive salivation with blood and mucous, hoarseness of voice (inflammation of epiglottis and larynx), diarrhea and pain at anus, suppression of urine and dehydration followed by shock. The vomitus is strongly acidic mixed with altered blood (brown, black or coffee color due to acid hematin), mucous and mucous membranes 2. CNS: Due to hypocalcemia, 2. CNS: Dyspnea, dizziness, 2. CNS: Not specific there is tetany characterized by delirium, convulsion, collapse, 3. Kidney: Oliguria and hematuria twitching of face and extremities coma 4. RS: Respiratory distress due to with tonic muscle spasm, cramps 3. Kidney: Carboluria characteritrickling of vomitus or leakage of and convulsions, with positive zed by hematuria and oliguria, acid Chvostek’s sign and Trousseau with casts in urine, which on exposed to air for 20–30 sec sign12 3. Kidney: Oxaluria characterised turns greenish due to the by hematuria and oliguria oxidation of its metabolic with calcium oxalate crystals product like hydroquinone in urine which is octahedral and pyrocatechol in shape. 4. These metabolites may get deposited in cartilages and ligaments or cornea3/sclera12 producing dark pigmentation— called ochronosis 5. Pupils constricted

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Forensic Toxicology: A Comparative Approach

Chvostek’s sign:23 When the facial nerve is tapped in front of tragus the facial muscles on the same side of the face will contract momentarily (typically a twitch of the nose or lips) because of hypocalcemia Trousseau sign:23,24 There is spasm of the muscles of the hand and forearm. The wrist and metacarpophalangeal joints flex, the DIP and PIP joints extend, and the fingers adduct (Fig. 4.7).

Fig. 4.7: Hand being held similar to Trousseau signs in latent tetany due to hypocalcemia Treatment 1. Emetics 2. Gastric lavage with calcium lactate (2 TSF), chalk, CaO. Warm water should not be used since it will dissolve oxalic acid 3. Purgatives and demulcents 4. Antidotes: Chalk powder, lime or wall scrapping (all contain calcium carbonate) can be given orally or 10 ml of 10% calcium gluconate is given IV5 5. Supportive: IV fluids—25% glucose; acidosis—NaHCO3 6. Restrict Na/K salts11

Treatment 1. Emetics 2. Gastric lavage with sodium/ magnesium sulfate solution25 3. Demulcents 4. Antidotes:25 Sodium/ magnesium sulfate 5. Supportive: IV fluids—25% glucose acidosis—NaHCO3 Digitalis for circulatory shock Artificial respiration + oxygen inhalation 6. For methemoglobinemia: If >30%—methylene blue (1–2 mg/kg) If >70%— exchange transfusion.25

Treatment 1. Emetics 2. Gastric lavage 3. Demulcents 4. Antidotes: Not specific 5. Supportive: IV fluids—25% glucose acidosis—NaHCO3 Artificial respiration + oxygen inhalation

PM findings

PM findings

PM findings

1. Local: Skin irritation with 1. whitish or yellowish 2. discoloration12, 20 2. MM of mouth/tongue—corroded, 3. swollen/sodden, bleached appear whitish/yellowish12 3. Stomach: Wall: Soft, swollen MM: Congested, desquamated, hemorrhagic, Scalded yellowish12 but becomes brownish due to acid hematin Contains: Brownish, blood mixed with mucus

Local: Skin necrosis, gangrene MM of mouth/tongue—corroded, first appear greyish white Stomach: Wall: Tough, thick, leathery brown,—“Leather bottle appearance”. (Fig. 4.9) MM: Congested, desquamated, hemorrhagic Contains: Brownish, blood mixed with mucus + Phenolic Smell

1. Local: Nil 2. MM of mouth/tongue, lipscorroded 3. Stomach: Wall: Soft, swollen MM: Congested, desquamated, hemorrhagic Contains: Brownish, altered blood + mucus shreds + vinegar smell 4. All visceral organs are congested 5. Kidneys are congested 6. Respiratory tract—congested, inflamed due to leakage of acid in RT. Lungs edematous

Corrosives

61

4. All visceral organs are congested 4. All visceral organs are congested 5. Kidneys are congested with 5. Kidneys are congested, enlarged presence of calcium oxalate and cortical hemorrhagic crystals 6. Surrounding structure/organs 6. Visceral organs show cloudy appeared necrosed and areas due to deposition of hardening with greyish white calcium oxalate staining of the viscera Preservation of viscera: V1 + V2 Preserved in: Rectified spirit

V1 + V2 preserved in saturated salt solution and not in rectified spirit

V1 + V2 preserved in saturated salt solution and not in rectified spirit

Medicolegal (ML) aspects 1. Suicide: Sometimes used for suicide 2. Homicide: Rarely used 3. Accidental poisoning: Mistaken with magnesium or zinc sulfate (Table 4.1) in children. 4. For forgery purpose: It is used to erase writing and signature5

ML aspects 1. Suicide: Commonly used for suicide (household poison) 2. Homicide: Rarely used where it is mixed with rum 3. Accidental poisoning: Mistaken with drakshasava (Ayurvedic drug), usually in children, chronic exposure due to its use or industrial exposure 4. Abortifacient: Used to procure criminal abortion

ML aspects 1. Suicide: May be used for suicide (household poison) 2. Homicide: Rarely used— detectable smell 3. Accidental poisoning: Mostly in children when taken by mistake, chronic industrial exposure

Diagnosis 1. Chemical test:12,21 1 ml of 1. Chemical test:5,11 10% Ferric Chloride + 10 ml BaCl2 + Oxalic = white Barium Oxalate crystals urine containing Phenol  2. Blood: Low serum calcium blue color substance level 2. Urine test-carboluria 3. Typical odor

Fig. 4.8: Corrosion around mouth in carbolic acid

1. Chemical test: Acid + drop of phenophthalein pink color + drop of 0.1 N NaOH pink color disappears 2. Typical odor

Fig. 4.9: Stomach in carbolic acid: Tough, thick and leathery bottle appearance

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Forensic Toxicology: A Comparative Approach

Fig. 4.10: Burns due to fall of sulfuric acid

Fig. 4.11: Blackish corrosion of skin due to consumption of sulfuric acid

Fig. 4.12: Corrosion of tongue, epiglottis and esophagus due to consumption of hydrochloric acid

Fig. 4.13: Black corrosion of tongue, epiglottis and esophagus due to consumption of sulfuric acid

Fig. 4.14: Blackish corrosion of stomach in sulfuric acid poisoning

Fig. 4.15: Trickling mark of acid over legs

Corrosives

63

Table 4.1: Difference between oxalic acid and magnesium sulfate and zinc sulfate Differences

Oxalic acid

Magnesium sulfate (epson salt)

Zinc sulfate

1. 2. 3. 4. 5. 6.

Sour Acidic Vaporizes Effervescences, no ppt. Removed

Bitter Neutral – White ppt. –

Bitter Acidic – White ppt. –

Taste Reaction On heating With NaCO3 Stain Figure

ALKALIES

Examples 1. Hydroxide: Ammonium, potassium, sodium, calcium. 2. Carbonate: Ammonium, potassium, sodium. Source: Industries, laboratories. Uses, fatal dose and period (Table 4.2) Properties • • • •

Most of these occur as white powder. Odorless Burning irritating taste Ammonium hydroxide is a liquid, having ammoniacal smell. • Hygroscopic in nature11

Fig. 4.17: Sodium hydroxide (caustic soda)

Fig. 4.16: Sodium carbonate (washing soda)

Fig. 4.18: Potassium hydroxide (caustic potash)

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Forensic Toxicology: A Comparative Approach

Table 4.2: Different alkalies and their uses Alkalis

Chemical formula

Common name

Uses12

Fatal dose Fatal period

Ammonium hydroxide NH4OH

Aqua ammonia Cleaning agents, plastic/ rubber manufacture

30 gm

24 hours

Sodium hydroxide

NaOH

Caustic soda

5 gm

24 hours

Potassium hydroxide

KOH

Caustic potash Drain cleaner, hearing aid batteries

5 gm

24 hours

Calcium hydroxide

Ca(OH)2

Slaked lime

White washing

–

–

Ammonium carbonate

(NH4)2CO3 Baker’s ammonia

Baking powder, fire extinguisher

30 gm

24 hours

Sodium carbonate

Na2CO3

Washing soda

Household cleaning agent, detergent

30 gm

24 hours

Potassium carbonate

K2CO3

Pearl ash

To make soap, in fire extinguishers

15 gm

24 hours

Drain cleaner, oven cleaner

Lye: It is a mixture of caustic soda and washing soda, used for washing purpose4

Mechanism of Action Locally: Act as corrosives. They dissolve the proteinand saponify fats, hence cause deeper burns. • Precipitates protein • Combine with fats to form alkaline soaps (saponification of fats) • Combine with protein to form alkaline proteinates (causes liquefaction necrosis).5 Clinical Features a. Intense burning pain in mouth and throat and abdomen with acrid, caustic and soapy taste, difficulty in speech and deglutition, dyspnea, vomiting, thirst, excessive salivation with blood and mucous, hoarseness of voice, diarrhea, suppression of urine and dehydration followed by shock. b. The vomitus is strongly alkaline mixed with altered blood (brown or black due to hematin), mucous and mucous shreds. Stool is mixed with blood and mucus. c. There is erosion of mucosa from lips to stomach, reddish brown color. There is also erosion of skin (greyish, soapy) necrotic area 5,12 along line of trickling of alkalies from angle of the mouth. d. Perforation may occur

e. With ammonia vapors—congestion and watering of eyes, sneezing, coughing and choking. There may be edema glottis, pneumonia and death. Treatment 1. Emetics and gastric lavage are contraindicated (perforation of stomach). 2. Drinking of plenty of plain water. 3. Weak vegetable acids like 3–5% acetic acid (vinegar), citric acid (lime/orange juice), 0.5% HCl 4. Demulcent drinks like milk, egg albumin, vegetable oil, ghee, butter, soap solution, etc. 5. Supportive treatment similar to acid burns. 6. Keep airway patent in ammonia inhalation 7. Antibiotic to prevent infection. 8. Alkalies injuries to skin and eye should be washed with water or saline for 20–30 minutes. Topical antibiotics and steroids may be helpful.12 Cause of Death Shock, perforation, peritonitis and laryngeal spasm, infection, stomach, esophageal stricture.

PM Findings 1. Gross corrosion of skin with soapy, greyish discoloration.

Corrosives

2. Corrosion of mucous membrane of mouth, tongue and lips with brownish discoloration present. 3. Stomach Wall: Soft, swollen MM: Desquamated, ulcerated, hemorrhagic, brownish (alkali hematin) Contents: Alkaline, altered blood, mucous, epithelium shreds 4. Gastric perforation may lead to peritonitis 5. Signs of repair with scarring present in late deaths. Medicolegal Aspects Poisoning by alkali is rare. 1. Suicide: Rare. 2. Homicide: Rare. 3. Accidental poisoning: Sometimes may occur due to mistaken for medicine, by children, or due to ingestion while pipetting the fluid usually in laboratory. 4. Vitriolage: They are commonly used for throwing on body, usually caustic soda. Chemical Test11 Hydroxides + AgNO3  yellow precipitates Carbonates + HCl  white precipitates IMPORTANT QUESTIONS

1. Classify corrosives with examples. Describe clinical manifestation, treatment and medicolegal significance of poisoning with anyone inorganic strong acid. Add a note on carboluria. 2. Describe vitriolage with its medicolegal importance. Describe clinical features, treatment, postmortem findings and medicolegal aspect in death due to carbolic acid poisoning. 3. Enumerate examples of organic corrosives. Describe clinical features, treatment, postmortem findings and medicolegal aspect in death due to oxalic acid corrosion. 4. Enumerate different alkalies. Describe clinical features, treatment, autopsy findings, medicolegal significance in

65

alkalies corrosion. Add a note on its chemical test. SPECIFIC LEARNING OBJECTIVES After reading this chapter, the reader should be able to:

• Classify corrosives with examples and their actions • Enlist various uses of different acids/ alkalies • Describe clinical features, treatment, postmortem findings and medicolegal aspects in HCl/H2SO4/HNO3 poisoning • Explain clinical features, treatment, postmortem findings and medicolegal aspects in carbolic/oxalic/acetic acid poisoning • Define vitriolage and explain its features, treatment and medicolegal aspect • Enumerate different chemical tests for strong acids/alkalies • Explain clinical features, treatment, postmortem findings and medicolegal aspects in alkalies poisoning • Delineate the difference between acid and alkali poisoning with respect to clinical features and treatment References 1. Sulfuric acid, concentrated (>51% and < 100%). Source: ILO-ICSC. http://www.ilo.org/dyn/icsc/showcard. display? p_version=2&p_card_id=0362 Description: International Chemical Safety Cards (ICSC) are data sheets intended to provide essential safety and health information on chemicals in a clear and concise way. © ILO and WHO 2017 2. Sulfuric acids in: PubChem CID: 1118. https:// pubchem.ncbi.nlm.nih.gov/compound/sulfuric_ acid#section=Top. Assessed on 18-11-2018. 3. Bardale R. Principles of Forensic Medicine and Toxicology. 1st edn, Jaypee Brothers Medical Publishers (P) Ltd: New Delhi. 2011: 437–44. 4. Dikshit PC. Textbook of Forensic Medicine and Toxicology. 2nd edn, PEEPEE Publisher and Distributors (P) Ltd. New Delhi. 2014: 474–81. 5. Reddy KSN, Murthy OP. The Essential of Forensic Medicine and Toxicology. 32nd edn, Om Sai Graphics: Hyderabad. 2013: 503–9.

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6. Nitric acid in PubChem CID: 944 https:// pubchem.ncbi.nlm.nih.gov/compound/ nitric_acid#section=Top 7. Nitric acid (>70% in water). Source: ILO-ICSC http://www.ilo.org/dyn/icsc/showcard. display?p_version=2&p_card_id=0183 Description: International Chemical Safety Cards (ICSC) are data sheets intended to provide essential safety and health information on chemicals in a clear and concise way. © ILO and WHO 2017. 8. O’Neil, MJ (ed.). The Merck Index—An Encyclopedia of Chemicals, Drugs, and Biologicals. Whitehouse Station, NJ: Merck and Co., Inc., 2006., p. 1138. 9. Hydrochloric Acid In: PubChem CID: 313. https://pubchem.ncbi.nlm.nih.gov/ compound/hydrochloric_acid#section= Physical-Description 10. Hydrogen chloride. Source: ILO-ICSC. http:// www.ilo.org/dyn/icsc/showcard.display? p_version=2&p_card_id=0163. Description: International Chemical Safety Cards (ICSC) are data sheets intended to provide essential safety and health information on chemicals in a clear and concise way. © ILO and WHO 2017. 11. Nandy A. Principles of Forensic Medicine. New Central Book Agency (P) Ltd: Calcutta, 2nd edn Reprint, 2004: 455–66. 12. Pillay VV. Textbook of Forensic Medicine and Toxicology. Paras Medical Publisher: Hyderabad, 17th edn, 2016: 497–520. 13. Claydon SM. An Acid Bath Murder. Acta Medicinæ Legalis Vol. XLIV 1994 pp 231–3. 14. Modi NJ. Examination of mutilated bodies or fragments. In: Modi’s Textbook of Medical Jurisprudence and Toxicology. NM Tripathi Private Ltd: Bombay. 20th edn, 1977: 78–9.

15. Singhal SK. Singhal’s Toxicology at a glance. 9th edn, National book depot: Mumbai. 41–9. 16. Qualitative analysis test for identifying organic functional groups of homologous series of molecules identification—for anions identifying negative ions hydroxide (alkalis) identification. http://www.docbrown.info/page13/ ChemicalTests/ChemicalTestsa.htm#Sulphate. 17. Criminal Law Amendment Act, 2013. 18. Reddi PR. Section 320 IPC. In: Criminal major Acts. 28th edn, Hyderabad: Asia Law House. 2018: 156. 19. Rentoul Edgar, Smith Hamilton. Toxic Hazards. In: Glaister’s Medical Jurisprudence and Toxicology. 13th edn, 1973. Churchill Livingstone: Edinburgh. 517–709. 20. Oxalic Acid In: PubChem CID: 971. https:// pubchem.ncbi.nlm.nih.gov/compound/oxalic_ acid#section=Color 21. Phenol in: PubChem CID: 996. https://pubchem. ncbi.nlm.nih.gov/compound/phenol#section= Physical-Description 22. Acetic Acid In PubChem CID: 176. https:// pubchem.ncbi.nlm.nih.gov/compound/acetic_ acid#section=Boiling-Point 23. Jesus JE, Landry A. Images in clinical medicine. Chvostek’s and Trousseau’s signs. The New England Journal of Medicine. 2012; 367 (11): e15. doi:10.1056/NEJMicm1110569. PMID 22970971. 24. Kumar, Abbas, Fausto. Pathologic Basis of Disease, 7th edition. Philadelphia: Elsevier-Saunders, 2005. 1188. 25. Barclay PJ. Phenols. In: Viccellio P (ed). Handbook of Medical Toxicology. 1st edn, 1993. Little, Brown and Company: Boston. 264–70.

5 Mechanical Irritants Mechanical irritants are the substances which causes irritation of the GIT at the site of contact. As such they are not poisons and do not cause any toxic effect. Glass powder, hair and fiber, diamond powder and metallic chips/pins are the examples of mechanical irritants (Figs 5.1 to 5.6).

MECHANICAL IRRITANTS 1. Glass powder/broken glass pieces

2. Hair and fibers

Bigger pieces can cause injury and hemorrhage in GIT. But smaller pieces fortunately do not get adhered to the wall of GIT and rather pass out the whole length of the tract by peristaltic movement1 Medicolegal aspects a. Accidental: Usually with jam, jelly, etc. contaminated with broken piece of their container. It also occurs to showmen while performing their show and may face problem b. Homicidal: May be used, where it is mixed with food/drink c. Cattle poisoning: Occasionally used.2

3. Diamond dust or powder

They may stick on the wall of stomach and intestine and remains undigested in the stomach. The hair ball may cause irritation (inflammation and pain) and lead to ulceration, GIT bleeding, perforation and obstruction.3 This collection of mass of hair in the stomach is called Trichobezoar. (Phytobezoar is due to collection of vegetable fibers in the stomach, particularly in patients who have gastric stasis.)4 Medicolegal aspects: a. It is almost exclusively found in female psychiatric patients, often young due to ingestion of hair.4 b. Homicidal: Very rare, where it is mixed with food 4. Metallic chips/nails and pins

It is really harmful due to the presence of minute spike on the surface of the diamond powder. These spikes get stuck and impregnated the wall of intestine and cause perforation, hemorrhage, inflammation and peritonitis.

Minute piece do not pose any problem but bigger piece may cause injury, hemorrhage and perforation of GIT. But the sharpness of the corner of metal piece is reduced due to the action of digestive enzymes.1

Medicolegal aspects a. Accidental: Poisoning may occur due to chronic exposure to diamond cutters

Medicolegal aspect Accidental: Mostly to children and also to magician (showmen) while performing their show

b. Homicidal: Used in ancient period by slow poisoning the king c. Suicidal: Rarely used 67

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Forensic Toxicology: A Comparative Approach

Fig. 5.1: Diamond powder

Fig. 5.2: Metallic chips

Fig. 5.3: Nails/pins

Fig. 5.4: Glass pieces

Fig. 5.5: Hair

Fig. 5.6: Fibers

Mechanical Irritants

69

Treatment of mechanical irritant poisoning 1. Bulky foods like banana, mashed potato, boiled rice, etc. 2. Demulcents: Starch, milk, barley water, oil, ghee, butter, egg albumin, etc. 3. High fiber diet, Metamucil or lactulose.5 4. Removal of swallowed foreign body through upper gastrointestinal endoscopy is also safe.5 5. Surgical intervention if required.

IMPORTANT QUESTIONS

1. What are mechanical irritants? Describe clinical manifestation, treatment in case of ingestion of anyone of mechanical irritant. Write its medicolegal aspect. 2. Enumerate mechanical irritants. Describe hair and fiber as mechanical irritant with its medicolegal significance. Write treatment in mechanical irritant. 3. Describe Trichobezoar and Phytobezoar with its medicolegal aspect. SPECIFIC LEARNING OBJECTIVES

After reading this chapter, the reader should be able to: • Enumerate different mechanical irritants with their examples and medicolegal aspects • Recognize the treatment of mechanical irritant poisoning

References 1. Nandy A. Principles of Forensic Medicine. New Central Book Agency (P) Ltd: Calcutta, 2nd edn Reprint, 2004:467–74. 2. Reddy KSN, Murthy OP. The Essential of Forensic Medicine and Toxicology. 32nd edn, Om Sai Graphics: Hyderabad. 2013: 521–3. 3. Levy NEJM, Levy Ronald M, Komanduri, Srinadh M. Trichobezoar. New England Journal of Medicine. 2007; 357 (21): e23. doi:10.1056/ NEJMicm067796. PMID 18032760. 4. Williams NS, Bulstrode CJA, O’connel PR (editors). Bailey and Love’s Short Practice of Surgery. 25th edn, Edward Arnold (publishers) Ltd: United Kingdom. 2008: 1077. 5. Al Shehri GY, Al Malki TA, Al Shehri MY, Ajao OG, Jastaniah SA, Haroon KS, Mahfouz MM, Al Shraim MM. Swallowed foreign body: Is interventional management always required? Saudi J Gastroenterol. 2000; 6:84–6.

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6

Non-Metallic Inorganic Chemical Irritants

These are the inorganic chemicals which not only exert their toxic effect on contact but also cause systemic poisoning. Phosphorus and halogens like iodine, chlorine, bromine, and fluorine are the examples of nonmetallic inorganic chemical irritant.

PHOSPHORUS

with skin. Red or brown phosphorus is n o n - toxic, inert and is prepared when white phosphorus is heated at a temperature of 280 o C, in the atmosphere of nitrogen (Table 6.1).

Properties and uses:1, 2 It exists in 2 forms— white or yellow and brown or red (Figs 6.1 and 6.2). White phosphorus is highly toxic and poisonous, causes burns when contact

Table 6.1: Difference between white and red phosphorus Differences1

Yellow phosphorus

Red phosphorus

Color

White, which on exposure to air becomes yellow

Red or brown

Appearance

Crystalline, translucent, soft, waxy, cylindrical

Amorphous, solid

Smell

Garlicky

Odorless

Taste

Garlicky

Tasteless

Luminosity

Luminous in dark

Non-luminous

Exposed to air

Ignites at 30oC and emits white fumes

Inert, non-fuming

Storage under water

Required

Not required

Toxicity

Highly toxic

Non-toxic

Uses

• It is used in chemicals, fertilizers, manufacture of phosphates and organophosphorus, rodenticide, insecticide. • It is also used in fireworks and gunpowder (smoke bombs and incendiary bullets), i.e. firearm ammunition.

• It is used on the sides of matchbox, where it is mixed with glass. • It is also used in matchstick head, where it is mixed with potassium chlorate [KClO3] and antimony sulphide [AnS].

Initially, white phosphorus was being used for the manufacture of Lucifer Matches, but due to its toxicity, it was banned in European countries2 after 1872 and present day safety match came into being after 1910.

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Non-Metallic Inorganic Chemical Irritants

Fig. 6.1: White phosphorus

71

Fig. 6.2: Brown phosphorus

Mechanism of action Locally, it destroys or burns the tissue (skin/ mucosa) on contact. It is a protoplasmic poison3, hampers tissue oxidation and causes fatty infiltration and necrosis4, 5 1. In acute poisoning: It causes hepatic dysfunction resembling ischemia known as necrobiosis, which results in disturbance in carbohydrate and fat metabolism 2. In chronic poisoning: There is excessive bone formation at the epiphyseal end (sequestration) with necrosis 3. Phosphine (PH3) causes respiratory distress Fatal dose: 60–120 mg

Fatal period: Variable, 12 hours to 1 week

Absorption, metabolism, excretion Absorbed through mucous membrane, quickly when stomach is empty or contains fatty foods. After absorption, it is distributed in all the organs and metabolized to hypophosphate and excreted through urine. Small part is excreted as such through feces and respiration Clinical manifestation depends upon 1. Dose 2. Period of exposure 3. Nature/type of poison 4. Routes: Contact/ingested/inhaled I. Acute phosphorus poisoning 1. Local: Necrosis of epidermis of skin after 1–2 days of its contact. Burned when ignited and becomes ulcerated (very painful and heals slowly) 2. GIT: Burning pain, vomiting, diarrhea, garlicky smell, intense thirst, salivation, and abdominal pain, followed by dehydration Vomitus and stool is dark, garlic smell, luminescence 3. CNS: Headache, insomnia, vision impaired, deafness, restlessness, delirium, tremor, convulsion, coma

II. Chronic phosphorus poisoning It occurs due to i. Exposure/inhalation of fumes in industries where phosphorous is used ii. Consumption of sea fish containing high quantity of phosphorus There is a triad of manifestation 1. GIT/general disturbances: Nausea, vomiting, loss of weight/appetite, pain in abdomen, alternate constipation and diarrhea, irritability, fatigability, lack of interest/concentration, weakness

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Forensic Toxicology: A Comparative Approach

Acute phosphorus poisoning

Chronic phosphorus poisoning

4. Liver: Jaundice, pruritis, bleeding points, with hepatosplenomegaly 5. Kidney: Oliguria, albuminuria, hematuria, with sugar and bile salt present 6. Bleeding from gums, nose, in skin, and under surface of visceral organs 7. Priapism6 (painful persistent erection of penis) 8. The patient usually presents with acute hepatic failure, coagulopathy, deranged liver function and acute renal failure.7 9. There is also decrease granulocyte count and bone marrow biopsy shows considerable decrease in cellular mass with degenerative changes.8

2. Cirrhosis of liver 3. Phossy jaw:9 It is the necrosis of mandible10 and sequestration (due to increased bone formation) and discharge of foul smelling pus by sinus formation. It is seen in 3% of industrial workers exposed to phosphorus. It is characterized by: • Pain/swelling/loosening of teeth with osteomyletis and necrosis of lower jaw with multiple sinuses discharging foul smelling pus. • Failure of dental socket to heal when teeth fall with inflammation of mucous membrane • Affected bone glowed greenish white color in dark11

Treatment: 1. Emesis 2. Stomach wash with antidote: 0.1% CuSO4 (forms copper phosphide) 0.5% KMnO4 (oxidizes phosphorus to phosphates) 3. Demulcents are contraindicated as they dissolve phosphorus 4. Non-fatty purgatives—MgSO4 5. Restriction of fats, demulcents, morphine due to liver damage 6. Dehydration or shock: IV fluids and glucose 7. Vit K, B-complex and vit C—hypoprothrombinemia 8. For external lesion: Washing with warm water or 1% CuSO4 solution, followed by application of bland and antibiotic ointment12

Treatment: 1. Prevent further exposure 2. Regular dental care: Mouthwash with NaHCO3 3. Plenty of oral calcium 4. Protect liver 5. Prevent intercurrent infection 6. Use of exhaust fans in working area 7. Working area sprayed with turpentine oil vapor

PM findings: 1. Locally, skin-necrosis, ulcerated 2. Mucous membrane of mouth eroded 3. Gum swollen with bleeding points 4. GIT stomach wall—soft, swollen; MM—eroded, desquamated, hemorrhagic; Contents—dark, garlic smell, luminous 5. Liver: In early stage, it is enlarged, soft, friable, greasy due to fatty degeneration (necrobiosis). In late stage it is shrunken, leathery, gritty, dirty yellow due to necrosis (acute yellow atrophy) (Table 6.2) 6. Yellowish discoloration of skin and petechial hemorrhage 7. Kidneys: Tubular degeneration 8. Fatty degenerative changes in heart and kidney

PM findings: 1. Phossy jaw 2. Liver cirrhosis 3. Poor oral hygiene

Table 6.2: Liver findings in phosphorus poisoning and acute yellow atrophy Phosphorus poisoning

Acute yellow atrophy

Usually enlarged, may be contracted later

Smaller, irregular

Marbled color

Bright yellow color

Soft, friable, greasy

Very soft and friable

Fatty degeneration

Necrosis of cell

Non-Metallic Inorganic Chemical Irritants

73

Medicolegal aspects 1. Suicide: Not preferred (due to painful death) 2. Homicidal: Not used (due to its smell and taste) 3. Accidental poisoning: Children are attracted by luminosity, or when they chew the matchstick heads or side. It also occurs: • Due to industrial exposure. • Through consumption of rodenticidal agents containing phosphorus 4. Abortifacient: Used both locally or general administration 5. Arson:4,13 It is used for causing outbreak of fire without being suspected. For this, phosphorus is wrapped in moist cow dung or moist rag and is kept/thrown on the roof of a house. When dung/rag becomes dry, the phosphorus gets ignited, producing fire on the thatched roof 6. To destroy undesired letters that has been posted 7. It is also used to create smoke screen in war field14 so as to infiltrate in the enemy side. 8. Greek fire/Fenian fire15: In this, phosphorus dissolved in carbon disulfide may be thrown on other person or property with malicious intention. The phosphorus burst into flames when carbon disulfide evaporates.

Fig. 6.3: Iodine crystals

Fig. 6.4: Chlorine tablets

HALOGENS

IODINE POISONING

CHLORINE POISONING

Physical characteristics: Solid, bluish-black scaly shining crystals emitting violet vapors (Fig. 6.3).

Greenish yellow gas, pungent smell

Uses: 1. In radio-opaque dyes. 2. For dressing, e.g. tincture of iodine, Lugol’s iodine or povidone iodine.

Uses: 1. Chlorine tablets (Fig. 6.4) for water purification in well and swimming pool 2. Bleaching agent 3. Sewage treatment12

Fatal dose: ~ 2 gm

Fatal dose12: >50–100 ppm

Fatal period: 12–24 hours

Fatal period14: 5 min to 12 hours

Actions:

Actions:

• It precipitates the protein • Irritation of GIT and RT

• It is extremely active oxidizing agent causing destruction of organic tissue.12 • Irritation to GIT and RT: Combine with water to form HCl and hypochlorus acid.

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Forensic Toxicology: A Comparative Approach

Clinical features

Clinical features

There may be sudden death due to anaphylaxis in sensitive people or it may cause chronic poisoning (Iodism) due to exposure of its vapor over long period. • Inhalation of vapor causes increased nasal and bronchial secretions, salivations, conjunctivitis, parotitis with cough and dyspnea. • Burning pain in upper GIT with nausea, vomiting, abdominal pain, diarrhea. • Vomitus/stool is bluish or violet with smell of iodine. • Urine is scanty and reddish brown with albuminuria and painful micturation.14 • Cold calmy skin, fall of BP/respiration, weak pulse. • Headache, giddiness, muscle cramp, delirium, collapse, shock.

• Inhalation of gas causes increased nasal and bronchial secretions, salivations, lacrimation with cough and dyspnea. • It may also result in laryngeal edema, pulmonary edema. • Nausea, vomiting, abdominal pain, diarrhea with increased BP and respiration rate. • Vertigo, headache, ventricular ectopic beats and metabolic acidosis.12 • Chronic exposure may cause corrosion of teeth12 anemia, loss of weight and appetite, bronchitis and emphysema14

Treatment

Treatment 14

1. Emetics: Gastric lavage with 5% sodium thiosulfate or with starch or egg albumin 2. Demulcents

1. Removal of patient to fresh air 2. O2 inhalation + artificial respiration + suction of frothy fluid form air passage.14

3. Antidote:14 5% sodium thiosulphate 100–150 ml orally to reduce free iodine to nontoxic iodides. 4. Supportive: For shock, dehydration, low BP, glottic edema.

3. Supportive treatment for shock, dehydration, pulmonary edema, acidosis. 4. Nebulised sodium bicarbonate (3.75% solution) to neutralized the acid formed when chlorine comes in contact with water in air passage.12

PM findings i. Mucosa of upper GIT: Inflamed. ii. Stomach contents are blue and emit smell of iodine. iii. Degeneration of heart, liver and kidney.

PM findings RT: Massive pulmonary edema with denudation of epithelium. Peculiar odor of chlorine from brain ventricle All organs are congested

Medicolegal aspects 1. Suicide: Rare. 2. Homicide: Rare. 3. Accidental poisoning: When mistaken with KMnO4, tincture iodine. 4. Vitriolage: It is used for vitriolage.

Medicolegal aspects 1. Suicide: Not possible 2. Homicide: Rare 3. Accidental: Commonly due to domestic or industrial exposure. 4. It is used in World War I as chemical warfare agent.

IMPORTANT QUESTIONS

1. Write difference between yellow and red phosphorus. Add a note on phossy jaw. 2. Describe mechanism of action, clinical features, treatment, postmortem findings and medicolegal aspect in acute phosphorus poisoning.

3. Enumerate non-metallic chemical irritant. Write in brief about clinical findings in chronic phosphorus poisoning. 4. Describe clinical manifestations, treatment and medicolegal aspect in iodine or chlorine poisoning. Add a note on different uses of iodine and chlorine.

Non-Metallic Inorganic Chemical Irritants

SPECIFIC LEARNING OBJECTIVES

After reading this chapter, the reader should be able to: • Enumerate difference between white and red phosphorus • Understand the mechanism of action of phosphorus • Explain clinical manifestations, treatment and postmortem findings in acute phosphorus poisoning • Explain clinical manifestations, treatment and postmortem findings in chronic phosphorus poisoning • Understand the basis of phossy jaw with medicolegal aspect of phosphorus poisoning • Enlist the uses of iodine and chlorine • Describe clinical manifestation, treatment, postmortem findings and medicolegal aspect in iodine/chlorine poisoning References 1. Pubchem: Phosphorus. In:PubChem CID: 5462309. https://pubchem.ncbi.nlm.nih.gov/compound/ 5462309#section=Chemical-and-PhysicalProperties 2. Crass MF, Jr.. “A history of the match industry. Part 9” (PDF). Journal of Chemical Education. 1941; 18 (9): 428–31. 3. Tenenbein M. Position statement: Whole bowel irrigation. American Academy of Clinical Toxicology; European Association of Poisons Centres and Clinical Toxicologists. J Toxicol Clin Toxicol.1997;35:753–62. [PubMed] 4. Nandy A. Principles of Forensic Medicine. New Central Book Agency (P) Ltd: Calcutta, 2nd edn Reprint, 2004: 467–74. 5. Bardale R. Principles of Forensic Medicine and Toxicology. 1st edn, Jaypee Brothers Medical Publishers (P) Ltd: New Delhi. 2011: 445–8.

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6. Singhal SK. Singhal’s Toxicology at a glance. 9th edn, National book depot: Mumbai.2016: 50–1. 7. Mauskar A, Mehta K, Nagotkar L, Shanbag P. Acute hepatic failure due to yellow phosphorus ingestion. Indian J Pharmacol. 2011 May-Jun; 43(3): 355–6. doi: [10.4103/0253-7613.81500] 8. Tafur A J, Zapatier J A, Idrovo L A, Oliveros J W, Garces JC. Bone marrow toxicity after yellow phosphorus ingestion. Emerg Med J. 2004; 21: 259–60. doi: 10/1136/emj.2003.007880 9. Hughes J P, Baron R, Buckland D H, Cooke M A, Craig J D, Duffield D P, Grosart A W, Parkes PW, Porter A. Phosphorus Necrosis of the Jaw: A PresentDay Study: With Clinical and Biochemical Studies. British Journal of Industrial Medicine. 1962; 19 (2): 83–99. 10. Marx Robert E. “Uncovering the Cause of “Phossy Jaw” Circa 1858 to 1906: Oral and Maxillofacial Surgery Closed Case Files—case Closed”. Journal of Oral and Maxillofacial Surgery. 2008 66 (11): 2356–63. doi:10.1016/ j.joms. 2007.11.006. PMID 18940506. 11. Workshops of Horror. New Zealand Department of Labour. Archived from the original on 20 June 2007. https://web.archive.org/web/20070620223046/ http://www.osh.govt.nz/kidz/gore/jphossy. shtml 12. Pillay VV. Textbook of Forensic Medicine and Toxicology. Paras Medical Publisher: Hyderabad, 17th edn, 2016: 511–27. 13. Reddy KSN, Murthy OP. The Essential of Forensic Medicine and Toxicology. 32nd edn, Om Sai Graphics: Hyderabad. 2013: 521–3. 14. Dikshit PC. Textbook of Forensic Medicine and Toxicology. 2nd edn, PEEPEE Publisher and Distributors (P) Ltd. New Delhi. 2014: 522–7. 15. Naill W, Whelehan Niall (9 August 2012). The Dynamiters: Irish Nationalism and Political Violence in the Wider World, 1867–1900. Cambridge University Press. p. 58. ISBN 9781139560979. Retrieved 3 March 2018.

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Forensic Toxicology: A Comparative Approach

7

Irritants: Inorganic Metallic Poison

These are the inorganic metallic compounds causing local irritation to the GIT. It includes toxic compounds of the metals. From the forensic point of view, important inorganic metallic poisons include compounds of arsenic, lead, copper and mercury. Pure metallic form (Figs 7.1 to 7.4) of arsenic, mercury and copper is not poisonous and not absorbed through GIT, but their compounds (Tables 7.1 and 7.2) are toxic. Table 7.1: Toxic compounds of arsenic and lead Arsenic

Lead

1. Arsenic trioxide (sankhya, somalkhar): White amorphous powder, colorless, odorless, tasteless, sparingly soluble in water 2. Arsenic hydride (Arsine) (AsH3): Highly toxic gas, burns with blue flame, garlic smell 3. Copper arsenite (Scheele’s green) and copper acetoarsenite (Paris green): Greenish color powder 4. Arsenic trisulfide (orpiment, multani mitti, harital)—bright yellow solid 5. Arsenic bisulfide (Realgur)—brick red powder 6. Arsenic trichloride: Highly toxic liquid having pungent smell and irritant to eyes

1. Lead acetate, lead sub-acetate—white crystalline salt, sweet astringent taste (Fig. 7.2) 2. Lead carbonate—white fine dusty powder used in paints 3. Lead tetraoxide (vermillion, sindoor, shondoor)— scarlet/safron color crystalline powder (used on Hanuman idol) 4. Lead sulfide (surma, kajal)—black powder 5. Lead monoxide—brick red 6. Tetraethyl lead (added to petrol) 7. Other: Lead chloride, lead nitrate, lead chromate, lead bromide, lead iodide

Table 7.2: Toxic compounds of mercury and copper Mercury Copper 1. Mercuric chloride (corrosive action)—colorless 1. Copper sulfate (CuSO4—blue vitriol, blue stone)— crystalline powder, odorless, burning metallic greenish blue crystals/powder, odorless, metallic taste, highly toxic. Used in medicines, laboratories, taste, soluble in gastric juice, absorbed in water industries, and as preservatives. Mercurous 2. Copper subacetate (verdegris) chloride (ras kapoor) is non-toxic, used as purgatives. 3. Copper chloride—white crystals 2. Mercuric cyanide—used in medicine 4. Copper carbonate—white dusty powder 3. Mercuric sulfide—[vermillion, sindoor, kumkum, kunku]—scarlet red crystalline powder 4. Mercuric sulphate—white crystalline powder 5. Phenyl mercuric acetate—used as fungicidal agent and preservation of seeds Other: Mercuric nitrate, mercurous nitrate, mercuric cyanide, mercury fulminate, mercury thiocyanate and mercurochrome Mercury exists in three forms:1,2 1. Elemental mercury/vapor 2. Inorganic mercury (mercuric and mercurous salts) 3. Organic mercury (ethyl/methyl mercury, mercurochrome). 76

Irritants: Inorganic Metallic Poison

Fig. 7.1: Arsenic

Fig. 7.2: Lead

77

Fig. 7.3: Copper

Fig 7.4: Mercury

Table 7.3: Fatal dose and fatal period of metallic poison Metals

Fatal dose

Fatal period

Arsenic

White arsenic = 200 mg

24 hrs to 7 days

Lead

Lead acetate = 20 gm, Lead carbonate = 30 gm

24 hrs to 7 days

Mercury

Mercuric chloride = 400–500 mg

Few hrs to 3–7 days

Copper

Copper subacetate = 15 gm, Copper sulphate = 30 gm

Few hrs to 3–7 days

Table 7.4: Source and uses of metallic irritant poison Arsenic

Lead

Mercury

Source: Industrial, domestic, commercial, agricultural

Source: Industrial, commercial, domestic

Source: Industrial, Source: Industrial, commercial, domestic commercial, domestic, agricultural

Copper

Arsenic is also found in soil and air,3 drinking water,4 sea fish and crustaceans5 Uses: • Depilatory/cosmetic agents • Paints, calico printing, Fruit spray • Colouring agents—toys • Insecticidal, weed killer, rodenticide • In fly paper/powder • In medicine—as Fowler’s solution6 in intermittent fever, general tonic, syphilis.

Uses: • Water pipes • Batteries • Paints, hair dye • Vermillion • Petrol • Glass blowing on the surface of ceremic articles • Pencil lead contains a mixture of graphite and clay, and not lead • Projectiles—bullet • Shielding from radiation

Uses: • As preservatives Vermillion • BP apparatus • Thermometer • Medicine, antiseptic and disinfectant • Snake tablet (Mercury Thiocyanate) in Diwali • Amalgam (dental filling) • Embalming • Fingerprint powder

Uses: Copper sulphate • Emetic agent • Antidote for phosphorous • Paints • Laboratory—test for fragility of RBC • Coloring agents—used to impart colour to peas, vegetable, stone • It is used as fungicide, and pesticide • Household appliances— copper utensils • Copper IU devices

Mechanism of action of metallic irritant7 1. Inhibits sulphydryl group of enzymes, thereby interfering with cell metabolism and oxidation. 2. Interfere with mitochondrial oxidative phosphorylation.

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Forensic Toxicology: A Comparative Approach

ARSENIC

LEAD

Pure metallic arsenic is not poisonous and not absorbed through GIT.

Pure metallic lead is absorbed through GIT.

Absorption, distribution, and excretion • Absorbed through mucous membrane of GIT, intact skin, or respiratory tract • The absorbed inorganic arsenic undergoes methylation mainly in liver to monomethylarsonic acid and dimethylarsinic acid, which are excreted in urine. 6 • Deposited in liver, kidneys, bones, hair, nails. • Excreted through urine, hair and nail. Small amount is also eliminated through feces, saliva, bronchial secretions, and milk

Absorption, distribution, and excretion • Usually absorbed through GIT. Lead dust/fumes through respiratory track. Lead tetraoxide/ tetraethyl lead aboerbed through skin. • After absorption, it is stored in bones as phosphate and carbonate.8 • Lead is a cumulative poison and deposited in bones, liver and kidneys. • It is excreted through urine, bile and nails

ACUTE ARSENIC POISONING

ACUTE LEAD POISONING

Clinical features Clinical features • Burning sensation, metallic taste, difficulty in • Burning sensation, metallic taste, difficulty in speech speech and swallowing, excessive salivation, thirst and swallowing, excessive salivation, thirst with with abdominal pain, vomiting, diarrhea with abdominal pain, vomiting, diarrhea with painful painful defecation and micturition. This is followed defecation and micturition. This is followed by by dehydration, muscle cramps, convulsion, dehydration, muscle cramps, convulsion, collapse, collapse, and coma and coma – Vomiting initially contains stomach contents – Vomiting—curdy white (lead chloride) mixed with blood and finally mucoid, watery – Diarrhea—black (lead sulfide) with streaks of blood • Scanty urine containing lead, albumin, copro– Diarrhea initially contains foul smelling fecal porphyrin 3 (red colored urine).9 matter mixed with blood5 and finally colorless, • CNS manifestations: Headache, insomnia, odorless mucoid and watery like rice-water drowsiness, dizziness, muscular cramps, stool of cholera (due to rupture of vesicles tremor, convulsions, collapse, coma, rarely paralysis formed under the mucosa)9 • Scanty urine containing blood and albumin • There is jaundice, anemia, hepatomegaly. • Hematological abnormalities:5 Hemoglobinuria, intravascular coagulation, bone marrow depression, severe pancytopenia, and normocytic normochromic anemia and basophilic stippling. Treatment 1. Emesis 2. Stomach wash:6 With freshly prepared ferric oxide (45 ml FeCl2 + 15 gm MgO)—filtering the ppt 3. Demulcent 4. Purgatives: Magnesium sulfate 5. Antidotes: BAL10/ferric oxide6 6. Supportive: For shock/dehydration Liver protection—vitamin/amino acids Renal failure—dialysis Blood transfusion, if required

Treatment 1. Emesis 2. Stomach wash:6 With magnesium/sodium sulfate (forms insoluble lead sulfate) 3. Demulcent 4. Purgative: Mg/Na sulfate 5. Antidotes: Calcium edetate/BAL or penicillamine or Mg/Na sulphate 6. Supportive Shock/dehydration—IV fluids Liver protection—vitamins D, and C/Thiamine Renal failure—dialysis Pain in abdomen—morphine Abdominal colic—calcium gluconate and atropine

Irritants: Inorganic Metallic Poison Antidote

79

Antidote 6, 8

1. Chemical: Sodium sulfate and magnesium 1. Chemical: Freshly prepared ferric oxide precipitate (prepared by adding 45 ml ferric sulfate chloride and 15 gm magnesium oxide then 2. Pharmacological10: Calcium edetate CaNa2 EDTA filtering the precipitate). Dose is 15 gm ppt in (Calcium disodium ethylene diamine tetra acetic glass of water. It forms ferric arsenite—which is acid), it excretes lead from circulation and bones. a harmless salt For dose: Refer to Chapter 1: Chelating agents BAL or penicillamine are also used. 2. Pharmacological:10 BAL, dimercaptosuccinic acid (It forms BAL—arsenic complex that is excreted out by the kidney). Dimercaprol is considerably more toxic than Succimer or Penicillamine PM findings • MM of mouth/esophagus—inflamed.

PM findings • MM of mouth—inflamed

• Stomach • Stomach: Red-velvety appearance11 Wall—soft, swollen Wall—soft, swollen MM—inflamed, hemorrhagic, and reddened MM—congested, greyish, sometimes eroded Contents—blood with mucous shreds present Contents—curdy white material arsenic powder or watery fluid mucoid and blood • Visceral organs congested streaks • Large intestine: Stools are black • Surrounding viscera—soft, inflamed, congested. • Visceral organs congested • Large intestine: Contains mucoid, watery material • Heart—subendocardial hemorrhage • Hemorrhages on larynx, trachea, lungs and abdominal organs • Usually, it retards decomposition. In decomposed body, yellowish discoloration occurs in stomach and surrounding tissue due to the formation of arsenic sulphide in arsenic poisoning. [arsenic +H2S = arsenic sulphide]. CHRONIC ARSENIC POISONING It occurs due to: 1. Industrial or agricultural exposures. 2. Contaminated food or drinks. 3. Arsenical medicines 4. Consumption of repeated small doses. 5. Consumption of contaminated drinking water, particularly arsenic laced tube well water in early 1980s in West Bengal.12

CHRONIC LEAD POISONING (PLUMBISM, ALSO KNOWN AS SATURNISM): It occurs due to: 1. Inhalation of dust/vapors in people working in factories/industries (e.g. paint industry, plumbing, glass—blowers, electric wire industries, batteries, toys, hair-dye and gasolene industries)9 2. Contaminated food and drinks with lead (stored/ cooked in tins or lead vessels)6 3. Prolonged use of vermillion, dye and cosmetic containing lead 4. One who handled petrol

Clinical features:

Clinical features [C-LEAD-P]:

Stage I: General loss of health and gastrointestinal disturbances Irritability, fatigability, lack of interest and concentration, loss of weight and appetite, abdominal pain, alternate constipation and diarrhea, gums inflamed and tooth loosened

C  Constipation, colicky pain The colic is intermittent, spasmodic and relieved by pressure and is associated with constipation L  Lead line (Burtonian line6—bluish discoloration over gingival surface of gums)

``` \

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Forensic Toxicology: A Comparative Approach

Stage II: Nasolacrimal and bronchial catarrhal changes Inflammation of conjunctiva, with watering from eyes and nose, photophobia, hoarseness of voice, cough with expectoration. (Features as of common cold) Ulceration of nasal mucosa Stage III: Cutaneous/keratin involvement i. Pigmentation of skin: Rain-drop appearance— pin-point brownish pigmentation of the skin. MiIk rose complexion—generalized brownish pigmentation due to vasodilatation Dark pigmentation with thickening of palm and soles ii. Nails—brittle, ‘Mee’s lines’ present (transverse, white streak at growing part of nail) iii. Hair—dry, alopecia, pigmented (yellow or brown) Stage IV: Neurological involvement Headache, irritability, fatigability, lack of interest and concentration Tingling and numbness, tremor, cramps, muscle weakness and paralysis Other manifestations Liver damage—jaundice, pruritis Kidney damage—albuminuria, hematuria, renal failure Bone marrow aplasia and basophilic stippling of RBC

E  Encephalopathy: It leads to irritability, fatigability, lack of interest/concentration, delirium, convulsion, collapse, coma. A  Alopecia, anemia with punctate basophilia. Anemia is due to: i. Impaired hemesynthesis. ii. Increase fragility of RBC due to loss of potassium due to increase cell permeability8 iii. Antithrombin effect of lead leads to defective clotting There is also basophilic stippling of RBC due to condensation of iron containing RNA near mitochondria.8 The RBC shows dark blue spots due to metabolic products of porphyrin. Other features seen on peripheral smear examination are: a. Reticulocytosis b. Decreased platelets c. Increased monocytes d. Anisocytosis e. Poikilocytosis D  Degenerative effect, lead deposited. Degenerative effect on: Reproductive system—leads to sterility. CVS in arteries—hypertension. Kidneys—chronic interstitial nephritis. Peripheral nerves—peripheral neuritis. Eye changes—retinal stippling and optic atrophy leading to blindness. Lead is deposited beyond the epiphysis of growing end of long bones8 leading to abnormal development in children (lead osteopathy). P  Pallor (facial pallor due to vasospasm). P Palsy—due to degeneration of nerves and atrophy of muscles leads to tingling numbness, weakness, tremors, cramps, etc. and ultimately leads to wrist drop and foot drop due to paralysis of extensor muscles of wrist and foot

(Blue line of gums is also seen in mercury, copper, silver, iron, bismuth and thallium poisoning). Treatment: Chronic arsenic poisoning 1. Prevention of exposure 2. BAL/penicillamine 3. Vitamin B complex 4. Supportive

Treatment: Chronic lead poisoning 1. Prevent further exposure 2. Antidote: Calcium versenate—1 gm/day slow IV drip or BAL/penicillamine 3. Potasium iodide (1–2 gm) and potassium citrate remove lead from bones and circulation respectively.8 4. Supportive: Magnesium sulfate—for constipation Atropine sulfate for severe colic NaHCO3, vitamin D, calcium diet

Irritants: Inorganic Metallic Poison

81

PM findings (chronic arsenic poisoning) 1. Dehydration, jaundice, anemia 2. Degenerative changes in thoracic and abdominal organs and nerves 3. Bone marrow aplasia 4. Keratin/cutaneous changes: Skin pigmentation, Mee’s line in nails, alopecia, bone marrow aplasia

PM findings (chronic lead poisoning) 1. Emaciated 2. Blue lining over gums 3. Alopecia 4. Evidence of anemia 5. Degenerative changes in liver, kidney, heart 6. Bone marrow aplasia

Laboratory investigation Urine:8 Arsenic level of >100 microgram/day is suggestive of poisoning. It becomes positive within 6 hrs of poisoning and continuous for about 2 wks. Hair and nails:5 Arsenic level of >1 mg/kg body weight indicates acute poisoning, while 0.1–0.5 mg/kg on a hair sample indicates chronic poisoning.

Laboratory investigation Urine:6 Presence of coproporphyrin level >0.15 mg/day Blood:8 Lead level of >50 microgram per dL. X-ray shows higher density beyond epiphysis Blood:6,13 Basophilic stippling of RBC presents with elevated level of delta amino-laevulinic (ALA) acid in postmortem blood.

Blood: Basophilic stippling of RBC present Interpretation of arsenic in exhumed body In dead bodies recovered from graves, there is the possibility that either the arsenic from the body percolates to the soil or arsenic from the soil may imbibe the body. Hence, the presence of arsenic should be interpreted very carefully in exhumed body: 1. Arsenic absorbed during life usually consists of soluble salt forms.8 The inorganic pentavalent forms of arsenic is absorbed at higher rate than bivalent forms.14 2. If arsenic has gone from the body to the soil, then not only the concentration of arsenic will be more in the body, the concentration in soil below the body will be more than the soil on both sides of the body and over the top of the body.

Arsenic trisulfide

Copper arsenite

Medicolegal aspects: 1. Suicidal: Not preferred due to painful death. 2. Homicidal: Earlier it was the most popular and considered as ideal homicidal poison and signs and symptoms resemble that of cholera. But it has got great disadvantages as it is detected not only in decomposed body but also in the body ash7, 8 and there is also chemical test to detect the poison

Lead tetraoxide

Lead monoxide

Medicolegal aspects: 1. Suicide: Rare—long, painful 2. Homicide: Rare, detection in CA 3. Accidental: Due to chronic exposure, to children 4. Accidental chronic lead poisoning may also occur due to retained bullet in the body after firing.15–17 5. Abortifacient: Sometimes used to procure abortion 6. Cattle poison

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Forensic Toxicology: A Comparative Approach

3. Accidental due to i. Consumption of contaminated food and drinks, ii. Exposure while in agricultural field, or in industries iii. Its abuses8 4. Abortifacient for procuring criminal abortion 5. Cattle poison18 and as stupefying poison Preservation of viscera Preservation of viscera 1. Routine viscera 1. Routine viscera 2. Additional viscera like hair, nails and ends of long 2. Additional viscera like nails and ends of long bones are also preserved. A serial analysis of hair bones are also preserved. and nails gives an indication of arsenic toxicity. Abuses of arsenic:8 a. It is used as love philter—it increases the affection towards the giver. In ancient days, the wives used to administer arsenic to their husband to gain attraction of the husband in the wake of unhealthy competition amongst the wives b. Aphrodisiac purpose—it gives a sense of well-being and is used to increase sexual desire c. It is also used to improve the dark complexion d. Arsenophagists6—are the person who takes arsenic daily. They can tolerate unbelievable amount of arsenic without much harm. It leads to tolerance and addiction Differential diagnosis of arsenic poisoning 1. Cholera—the manifestation starts with diarrhea in cholera and vomiting in arsenic poisoning. (Table 7.5 for the differences). The stools are described as ‘rice water’ in cholera, and bloody rice water in acute arsenic poisoning due to presence of blood in GIT 2. Bacterial food poisoning—vomiting and diarrhoea occur within 15–30 min in arsenic poisoning while they are delayed by few hours in bacterial food poisoning. Table 7.5: Differences between arsenic poisoning and cholera Points

Arsenic poisoning

Cholera

1. Start with

Vomiting

Diarrhea

2. Vomitus contains

Blood and mucus

Mucus only, watery

3. Purging

After vomiting

Before vomiting

4. Stool

Rice watery with blood and mucus

Rice watery liquid

5. Tenesmus and anal irritation

Present

Absent

6. Metallic taste

Present

Absent

7. Motive

Present

Absent

8. Restricted to

Individual

Not restricted, affects many

9. Lab test

On CA, arsenic present

On hanging drop-darting motility of bacteria present

MERCURY (QUICK SILVER, PARA)

COPPER (TAMBA)

Pure metallic mercury is not poisonous as it is not absorbed through GIT. Mercury is a liquid metal, heavy, silvery and non-adhesive. Vapors of mercury are toxic and induce severe pneumonitis.1

Pure metallic copper is not absorbed through GIT and not poisonous6

Irritants: Inorganic Metallic Poison

83

Absorption, distribution, excretion • Absorption through GIT. The vapors and salts are also absorbed through RT, vagina (in vaginal douche), and bladder. • Distributed in liver, spleen, kidney, bone and brain (in phenyl mercuric acetate). Soluble forms get deposited in liver, spleen, kidney, intestines, heart, muscles and lungs. • Excreted in urine, bile, feces and body secretions.

Absorption, distribution, excretion • Absorbed through GIT • Distributed in liver, spleen, and kidney • Excreted in urine, bile, feces

ACUTE MERCURY POISONING

ACUTE COPPER POISONING

Clinical features • Local: Skin—corrosion. • MM of mouth and tongue: Corroded and is greyish-white in color6 • Burning sensation, metallic taste, difficulty in speech and swallowing, excessive salivation, thirst with abdominal pain, vomiting, diarrhea with painful defecation and micturition. This is followed by dehydration, muscle cramps, convulsion, collapse, and coma – Vomiting contains mucous with altered blood and shreds of mucosa – Diarrhea is blood stained with necrosed mucus shreds of colon • Scanty urine containing blood and albumin • General: Headache, tremor, deafness, scotoma, loss of memory, loss of appetite, fatigue • Inhalation of mercury vapors: Cough, dyspnea, salivation, stomatitis, gingivitis, conjunctivitis.

Clinical features • Anemia: Due to increase fragility of RBC causes hemolysis • Burning sensation, metallic taste, difficulty in speech and swallowing, excessive salivation, thirst with abdominal pain, vomiting, diarrhea with painful defecation and micturition. This is followed by dehydration, muscle cramps, convulsion, collapse, and coma – Vomiting is greenish blue—turns to deep blue with ammonia/NH4OH.6 – Diarrhea is greenish blue • Scanty urine containing blood, albumin • Liver damage: Jaundice

Treatment 1. Emesis: By lukewarm NaHCO3 solution, Ipecacuanha 2. Stomach wash:6 5–10% sodium formaldehyde sulfoxylate 3. Demulcent: Egg albumin, milk, gelatin, etc. 4. Purgatives, high colonic lavage 5. Antidote:10, 12 BAL/penicillamine 6. Supportive: Shock/dehydration—IV fluids Renal failure—NaHCO3/peritoneal, or hemodialysis Exchange tranfusion

Treatment 1. Emesis: There is no use of emetics. (Copper salts are potent emetics.) 2. Stomach wash:6, 12 1% Pot. ferrocyanide 3. Demulcent 4. Purgatives: Castor oil 5. Antidotes:10 BAL/penicillamine 6. Supportive: Diuretics Shock/dehydration—IV fluids Liver/renal damage—vitamin, AA, hemodialysis12 Exchange transfusion

Antidote a. Physical: Egg albumin (forms mercuric albuminate), demulcents, charcoal b. Chemical:6 5% solution of sodium formaldehyde sulfoxylate with 5% NaHCO3 c. Pharmacological: DMPS (2,3-Dimercapto-1propanesulfonate)—3 mg/kg IV over 5 min, 100 mg TID × 2 wks followed by QID for 6 weeks2,19 or DMSA (dimercaptosuccinic acid), an analog of BAL has high affinity for mercury.20

Antidote a. Physical: Demulcents (forms copper albuminate with proteins) b. Chemical:6,12 Potassium ferrocyanide (forms insoluble cupric ferrocyanide) c. Pharmacological:12 BAL followed by penicillamine

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Forensic Toxicology: A Comparative Approach

PM findings 1. Skin and MM of mouth, tongue, esophagus— corroded and greyish white. 2. Stomach: Wall—soft, swollen MM—desquamated, hemorrhagic, ulcerated, necrosis and greyish white/black Contents—altered blood and mucus shreds. 3. Intestines: Congested, ulcerated, and sometimes gangrenous. 4. Kidney: Swollen, nephritis. 5. Liver: Congested, central necrosis and cloudy swelling 6. Heart: Sub-endocardial hemorrhages

PM findings 1. MM of mouth, tongue and esophagus—greenish blue lining 2. Stomach: Wall—soft, swollen MM—desquamated, hemorrhagic, congested, greenish blue lining Contents: Greenish blue 3. Intestines: Hemorrhages and ulcerations, greenish blue lining 4. Greenish—blue froth at mouth and nostrils. 5. Liver: Jaundice

CHRONIC MERCURY POISONING (Hydrargyrism) It occurs due to: 1. Chronic exposure to people working in industry and laboratory 2. Repeated administration of multiple small doses of medicines containing mercury. 3. Contaminated food, drinks, and sea fish. Mercury is methylated under sea water and consumption of such fish causes chronic poisoning. (Minimata disease)21, 22

CHRONIC COPPER POISONING It occurs due to hemocromatosis: 1. Chronic industrial exposure 2. Consumption of vegetables colored with copper sulfate 3. Consumption of contaminated food and drink (stored/cooked in copper utensils—Wilson disease) due to deficiency of ceruloplasmin (2 hr/day for >6 days/week16; intermittent medical check up; proper washing of hands and face after spraying; immune-compromised/ill/injured person should avoid spraying. Table 8.4: Atropine and oximes in the treatment of different groups of insecticidal poisoning Groups Atropine Oximes Organophosphorus (OP)

Antidote

Antidote

Organochlorines (OC)

Do not give

No role in treatment

Carbamates

Antidote

Contraindicated

Pyrethroids

Given only if needed

No role in treatment

10

In OC: Do not give epinephrine or atropine unless absolutely necessary, because of the enhanced myocardial irritability induced by chlorinated hydrocompound, which predispose to ventricular fibrillation. Do not give oil-based cathartics/demulcent as they enhance absorption. PM findings 1. Characteristic odor (garlicky) near mouth 2. Frothing at mouth and nose—blood stained 3. Cyanosis of extremities 4. Constricted pupils 5. It resists decomposition and can be easily detected even in putrefied bodies 6. Stomach—garlicky or kerosene/turpentine like odor of solvent and content, mucosacongested, hemorrhagic 7. Pulmonary and cerebral edema 8. Froth in the respiratory tract 9. Visceral organs are congested

PM findings 1. Characteristic odor (chlorinated/pungent) 2. Discharge of bloodstained froth from nose and mouth 3. Cyanosis and s/o asphyxia 4. Dilatation of pupils 5. Detected even in putrefied bodies 6. Stomach—chlorinated or kerosene/turpentine smell of solvent and content, mucosa-congested, hemorrhagic 7. Lungs—congested, edematous, subpleural hemorrhagic spots 8. Froth in the respiratory tract 9. Visceral organs are congested, brain—edema. 10. Liver, kidneys, adrenal—fatty degeneration

A useful postmortem finding in insecticidal poisoning case infested with flies at mortuary is that some of these flies after settling on decomposed body may subsequently die and found on the body. In death during spraying of insecticide in the field, the nasal swab, blood and lung should be preserved for toxicological analysis. The insecticide poison may not be detected in routine viscera in such case and chemical analyser’s report is negative. ML aspects 1. Suicidal: Common in India both rural and urban areas 2. Homicidal: Not occur due to detectable smell of solvent. However, a few cases have been reported 3. Accidental: Mainly to manufacturer, packers, sprayers in the fields, and also due to contaminated food grains

ML aspects 1. Suicidal: Common, more in rural areas 2. Homicidal: Very rare where the smell of kerosene is masked by alcohol 3. Accidental: Usually in children, and one who handle the poison

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Forensic Toxicology: A Comparative Approach

Stomach in Insecticidal Poisoning (Courtesy—Dr. Barmate/Dr. Tumram) (Figs 8.1 to 8.6)

Fig. 8.1: Phorate poisoning (OP)

Fig. 8.2: Phorate granules

Fig. 8.3: Monocrotophos—Nuvacron poisoning (OP)

Fig. 8.4: Dimethoate—Rogar poisoning (OP)

Fig. 8.5: Endrin poisoning (OC)

Fig. 8.6: Endosulphan—thiodan poisoning

Agricultural Poison: Pesticides

CARBAMATES

101

PYRETHRINS AND PYRETHROIDS

They are as popular as organophosphates in their Pyrethrins are active extracts of the Chrysanthemum role as insecticides and share a number of similarities plant (Chrysanthemum cinerariaefolium), and include pyrethrum and piperonyl butoxide. Most mammals are resistant since they can rapidly metabolize and detoxify these agents. Properties They are available as liquids, sprays, dusts and powders

Properties They are available as liquids, sprays, dusts, powders, mats, and coils

Uses Apart from insecticidal use, these are used to kill insect and ants in household spray

Uses These compounds are used as insect repellants and insecticides in household sprays, mosquito coils, and mats They are also used to prevent pest infestation in granaries and in agriculture as pesticides

Fatal dose • Highly toxic: Carbaryl, carbofuran, methomyl, propoxur. • Moderately/slightly toxic: Aldicarb, carbendazim, triallate Fatal period: Uncertain

Fatal dose • Pyrethrum has an LD50 of over 1 gm/kg. • Most cases of toxicity are actually the result of allergic reactions

Action Carbamates (like organophosphates) are inhibitors of acetylcholinesterase, but carbamylate the serine moiety at the active site instead of phosphorylation.9 This binding is of reversible type and so the clinical features are less severe and of shorter duration.

Action Pyrethroids prolong the inactivation of the sodium channel by binding to it in the open state. Type II agents are more potent in this regard, and also act by inhibiting GABA-mediated inhibitory chloride channels

Clinical features:

Clinical features:12

Fatal period: Uncertain

• The clinical manifestations of carbamate poisoning 1. Skin contact: Dermatitis, blistering are very similar to organophosphate poisoning 2. Eye contact: Irritation but symptoms are less severe and of shorter 3. Inhalation: Rhinorrhoea, sore throat, wheezing, duration dyspnea • Salivation, lacrimation, sweating, vomiting, 4. Ingestion: Increased salivation, nausea, diarrhea, slow pulse, low BP, weakness, twitching, vomiting, abdominal pain, mouth ulceration, convulsion dysphagia. 5. Systemic effects: Headache, dizziness, fatigue, palpitation, chest tightness, vertigo, fasciculation, hyperthermia, altered mental status, convulsion, coma. Diagnosis 1. Blood cholinesterase level is decreased 2. X-ray may reveal the presence of certain radiopaque carbamates 3. Carbamates can be detected in serum, adipose tissue and urine by gas chromatography

Diagnosis 1. Blood cholinesterase levels are normal 2. ECG may demonstrate ST-T changes, sinus tachycardia, and ventricular premature beats 3. Thin layer chromatography

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Forensic Toxicology: A Comparative Approach

Treatment (Table 8.3):

Treatment (Table 8.3):

• Inj. PAM is contraindicated in cases of poisoning • Inj. PAM—no role in treatment. with carbamate compounds • Atropine is given only if needed for hyper• But, IV atropine is useful secretion and pulmonary edema In carbamate poisoning treatment: An important differentiating point from organophosphates is that oximes are generally not recommended, while atropine can be given. Pralidoxime is ineffective as an antidote to carbamate anti-ChEs (carbaryl, propoxur, physostigmine, neostigmine) in which case the anionic site of the enzyme is not free to provide attachment to it. It is rather contraindicated in carbamate poisoning, as it does not reactivate carbamylated enzyme, but it has weak anti-ChE activity of its own.6 Oximes given in carbamate poisoning leads to the production of carbamylated oximes which may be more potent acetylcholinesterase inhibitor than carbaryl itself.9 PM findings

PM findings

1. Characteristic odor (peculiar or kerosene like) near mouth

1. Characteristic odor (garlicky or kerosene like) near mouth

2. Blood stained frothing at mouth and nose

2. Blood stained frothing at mouth and nose

3. Cyanosis of extremities

3. Cyanosis of extremities

4. Stomach: Mucosa congestion with kerosene-like odor of contents

4. Stomach: Mucosa congestion with characteristic odor of contents

5. Pulmonary and cerebral edema

5. Pulmonary and cerebral edema

6. Froth in the respiratory tract

6. Froth in the respiratory tract

7. Generalized visceral congestion

7. Generalized visceral congestion

ML aspects

ML aspects

1. Suicidal: Usually

1. Suicidal: May occur

2. Accidental: Common

2. Accidental: Common in children due to consumption of mats and coils

Carbamate and Pyrethroids (Figs 8.7 to 8.13)

Fig. 8.7: Cypermethrin/allethrin

Fig. 8.8: Pyrethrum

Agricultural Poison: Pesticides

Fig. 8.9: Transfluthrin

Fig. 8.11: Carbendazim (carbamates)

103

Fig. 8.10: Cypermethrin

Fig. 8.12: Deltamethrin

Fig. 8.13: Fenvalerate

Rodenticidal Agents (Figs 8.16 and 8.17) ALUMINIUM PHOSPHIDE

ZINC PHOSPHIDE

Preparations: Alphos, Celphos, Phosfume, Phostoxin, Phosphotek, Quickphos, etc.

Preparations: Synphos, Ratol, Sudharshan

They are available as greenish grey tablets of aluminium phosphide urea and ammonium carbonate. They have garlic smell. On exposure to air, it releases phosphine,9 ammonia and carbon dioxide AlP + 3H2O  Al(OH)3 + PH3

It is a steel grey, crystalline powder with fishy smell. It also releases phosphine. It is used as fumigant to control insects and rodents ZnP + 3H2O  Zn(OH)3 + PH3

Action: It acts by blocking the cytochrome C oxidase enzyme and inhibiting oxidative phosphorylation which eventually leads to cell death.22,23 Fatal dose: One tablet (3 gm) Fatal period: 12–24 hours

Fatal dose: 5 gm Fatal period: 24 hours

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Forensic Toxicology: A Comparative Approach

Uses: For protecting stored grain (rice tablet)23, rodenticidal

• It is used as fumigant to control insects and rodents (rodenticidal)

Clinical features:22,24 Nausea, vomiting, diarrhea, epigastric pain, dizziness, restlessness, cyanosis, rapid respiration, with garlicky/fishy odor breath, dyspnea, tachycardia, cardiac arrhythmia, peripheral circulatory failure, convulsion, coma. Death is due to circulatory failure. Diagnosis: Garlicky odor, ECG changes (sinus tachycardia, ST-T wave changes, bradycardia, heart block), Silver Nitrate test:9,25 When a patient is asked to breath in and out through a piece of filter paper impregnated with 0.1N silver nitrate solution for 5–10 min, then the filter paper turns black due to the presence of phosphine in the breath which reduces silver nitrate to silver. This test is also positive for hydrogen sulphide. Treatment:9,22 1. Fresh air. 2. Stomach wash is not indicated—chance of release of PH3. 3. IV fluids, sodium bicarbonate and vasopressors for shock and acidosis. 4. Additionally, 1 mg of glucagon IV every 5–10 minutes until his blood pressure becomes control followed by 4 mg/hr slow IV infusion. Subsequently, digoxin (0.5 mg), magnesium sulfate (1 gm), calcium gluconate (1 gm), hydrocortisone (200 mg) given every 6 hourly with vit C (1000 mg), vit E (400 unit IM) and N-acetylcysteine 140 mg/kg orally as a loading dose followed by 70 mg/kg orally every 4–6 hrly for 4–5 days.9,22 5. Hemodialysis. PM findings: Garlicky/fishy smell in the stomach with mucosal haemorrhage (Figs 8.14 and Fig 8.15), visceral organs—congested; Liver and kidneys—necrotic changes; pulmonary edema, toxic myocarditis ML aspects

ML aspects

1. Suicide: Common, usually in Northern India24

1. Suicide: Commonly in young age.

2. Homicidal: Not used.

2. Homicidal: Not used

3. Accidental: Rare, usually in children.

3. Accidental: Rare, usually in children.

Fig. 8.14: Stomach in zinc phosphide poisoning

Fig. 8.15: Stomach in aluminium phosphide poisoning

Agricultural Poison: Pesticides

105

Fig. 8.17: Zinc phosphide

Fig. 8.16: Aluminium phosphide

Other Pesticides: Fungicidal and Herbicidal (Figs 8.18 to 8.22)

Fig. 8.18: Fungicidal (Devithiram)

Fig. 8.19: Fungicidal (Benomyl)

Fig. 8.21: Herbicidal (Glyphosphate)

Fig. 8.20: Herbicidal (Quizolofeb)

Fig. 8.22: Flowering stimulant (Nitrobenzene)

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Forensic Toxicology: A Comparative Approach

IMPORTANT QUESTIONS

1. Classify agricultural poisons. Describe mechanism of action, clinical features, treatment, laboratory diagnosis and autopsy findings of organophosphorus poisoning. 2. Classify pesticides. Describe clinical features, treatment and autopsy findings of organochlorine poisoning. 3. Classify insecticidal poisons. Describe clinical features, treatment and autopsy findings of carbamate poisoning. 4. Classify rodenticidal agents. Describe clinical manifestation, treatment and medicolegal aspect of rodenticidal poisoning. 5. How will you diagnose and manage a case of baygon poisoning? 6. How will you diagnose a case of insecticidal poisoning? Describe in brief about management of different insecticidal poisoning. SPECIFIC LEARNING OBJECTIVES

After reading this chapter, the reader should be able to: • Classify insecticidal poisons with their examples • Classify pesticides with their examples • Understand the mechanism of action of different insecticidal poisons • Enumerate different organophosphorus compounds and describe the clinical features, diagnosis, treatment, postmortem findings and medicolegal aspect of organophosphorus poisoning • Explain clinical features, diagnosis, treatment, postmortem findings and medicolegal aspect of organochlorine poisoning • Enlist various carbamate compounds and describe the clinical features, diagnosis, treatment, postmortem findings and medicolegal aspect of carbamate poisoning • Delineate the management of different insecticidal poisoning

• Classify rodenticidal agents and describe clinical features, treatment, postmortem findings and medicolegal aspect of aluminium/ zinc phosphide poisoning References 1. Seven farmers die, hundreds admitted to hospital in Yavatmal district after inhaling insecticide spray. The Indian Express. Dated 23/ Feb/ 2019. https://indianexpress.com /article/ cities/mumbai/maharashtra-insecticide-sprayseven-farmers-die-hundreds-admitted-tohospital-in-yavatmal-district-4866394/ 2. Thundiyil JG, Stober J, Besbelli N, Pronczuk J. Acute pesticide poisoning: a proposed classification tool. Bull World Health Organ 2008;86:205–9. [PubMed] 3. Raut Asawari, Pawar Atmaram, Kakane Bhagwan, Dave Priti, Shaj Kavya, Gulam Ali Jabeen. Toxicological Pattern of Poisoning in Urban Hospitals of Western India. J Young Pharm, 2017; 9(3):315–20. 4. All India Institute of Medical Sciences, New Delhi. National Poisons Information Centre. http://www.aiims.edu/en/departments-andcenters/central-facilities.html?id=167 (accessed 18 August 2016). 5. Siwach SB, Gupta A. The profile of acute poisoning in Haryana. J Assoc Physicians India.1995;13: 756–9. [PubMed] 6. Tripathi KD. Cholinergic system and drugs. In: Essential of Medical Pharmacology. Jaypee Brothers Medical Publishers (P) Ltd: New Delhi, 7th edn, 2014:99–112. 7. Organophosphate poisoning: diagnosis and treatment. https://www.openanesthesia.org/ organophosphate_poisoning_diagnosis_and_ treatment/ 8. Peter JV, Sudarsan TI, Moran JL. Clinical features of organophosphate poisoning: A review of different classification systems and approaches. Indian J Crit Care Med. 2014 Nov; 18(11): 735–45. doi: [10.4103/0972–5229.144017] 9. Pillay VV. Textbook of Forensic Medicine and Toxicology. Paras Medical Publisher: Hyderabad, 17th edn, 2016: 602–17. 10. Reigart JR, Roberts JR. Organochlorines. In: Recognition and Management of Pesticide Poisonings. 6th Ed., 2013. Published by: Office of Pesticide Programs, US Environmental Protection

Agricultural Poison: Pesticides Agency, Washington. Pg: 63–9. https:// www2.epa.gov/pesticide-worker-safety 11. Cohn WJ, Boylan JJ, Blanke RV, Fariss MW, Howell JR, Guzelian PS. Treatment of chlordecone (Kepone) toxicity with cholestyramine. Results of a controlled clinical trial. N Engl J Med. Feb 2 1978;298(5):243–8.

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synthetic pyrethroid insecticides. Environmental Health Perspectives. 1990;87:255–62.doi: 10.1289/ ehp.9087255. 19. Dikshit PC. Textbook of Forensic Medicine and Toxicology. 2nd edn, PEEPEE Publisher and Distributors (P) Ltd. New Delhi. 2014:587–96

12. Bradberry SM, Cage SA, Proudfoot AT, Vale JA. Poisoning due to pyrethroids. Toxicol Rev. 2005;24(2):93–106.

20. Zorawar Singh, Jasminder Kaur, Ravneet Kaur, Swarndeep Singh Hundal.Toxic Effects of Organochlorine Pesticides: A Review. American Journal of BioScience. 2016;4(3–1)11–8.

13. Aktar MW, Sengupta D, Chowdhury A. Impact of pesticides use in agriculture: their benefits and hazards. Interdiscip Toxicol. 2009 Mar; 2(1): 1–12. doi: [10.2478/v10102-009-0001-7]

21. Kukde HV, Ambade VN, Batra AK, Keoliya AN. Significance of serum cholinesterase level in organophosphorus poisoning. Medicolegal update 2012; 12(2):70–4.

14. FAO. Proceedings of the Asia Regional Workshop. Bangkok: Regional Office for Asia and the Pacific; 2005. 15. Gupta PK. Pesticide exposure—Indian scene. Toxicology. 2004;198:83–90. [PubMed]

22. Oghabian Z, Mehrpour O. Treatment of Aluminium Phosphide Poisoning with a Combination of Intravenous Glucagon, Digoxin and Antioxidant Agents. Sultan Qaboos Univ Med J. 2016 Aug; 16(3): e352–5. doi: [10.18295/squmj.2016.16.03.015]

16. Nandy A. Principles of Forensic Medicine. New Central Book Agency (P) Ltd: Calcutta, 2nd edn Reprint, 2004:491–7.

23. Mehrpour O, Singh S. Rice tablet poisoning: a major concern in Iranian population. Hum Exp Toxicol. 2010 Aug; 29(8):701–2. [PubMed] [Ref list]

17. Lotti M. Clinical toxicology of anticholinesterase agents in humans. In: Krieger R, editor. Handbook of pesticide toxicology. Volume 2. Agents. 2 edn. Academic Press; San Diego: 2001. pp. 1043–85.

24. Gurjar M, Baronia AK, Azim A, Sharma K. Managing aluminum phosphide poisonings. J Emerg Trauma Shock. 2011 Jul; 4(3):378–84. [PubMed] [Ref list]

18. J R Coats. Mechanisms of toxic action and structure activity relationships for Organochlorine and

25. Bardale R. Principles of Forensic Medicine and Toxicology. 1st edn, Jaypee Brothers Medical Publishers (P) Ltd: New Delhi. 2011: 490–9.

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9 Plant and Vegetable Irritants These are the organic irritants derived from poisonous plant and vegetables. There are various plants/ vegetables that are poisonous/toxic to human beings. The study of plant poison which produces toxic effect on human is called phytotoxicology and its poison is referred to as phytotoxins.1 Based on their toxic effects, poisonous plants are classified as: 1. Gastrointestinal irritant: Abrus, ricin, etc. 2. Neurotoxin: Opium, datura, cannabis, nux vomica. 3. Cardiotoxic: Aconite, olender, quinine, tobacco. 4. Contact poison: Poison ivy, sumac, mango, cashewnut. 5. Airborne allergic: Acer negundo (box elder). Some of the plants whose toxic part on ingestion causes gastrointestinal irritation are only included in this chapter. Vegetable irritants are Abrus precatorius, Ricinus communis, Croton tiglium, Semicarpus anacardium, Calotropis, Plumbago rosea, Capsicum.. Toxalbumin2 is the toxic protein present in some of the vegetable irritants. The action resembles the action of bacterial toxin, e.g. Ricin, Abrin, Crotin, Snake venom. It is antigenic in nature and capable of producing specific antibodies when injected into the body. It causes agglutination, haemolysis and cell destruction.2,3

Abrus precatorius

Ricinus communis

Croton tiglium

Synonyms: Rati, Gunj, Kunch, Crab eyes, Precatorius beans, Lucky beans

Synonyms: Castor, Arandi

Synonyms: Croton, Jamalgota

Toxic parts: Seeds. Seeds: Small beautiful, glossy bright red/brownish/faint yellow with black head, and weigh 102 mg

Toxic parts: Seeds. Seeds: Small/big (2 varieties) brownish oval glossy seeds with yellowish marking

Toxic parts: All part of plant (max. conc. in oil and seeds) Seeds: Small dark brown oval matt/ dull dusty seeds

Uses 1. Decoration purpose 2. To weigh gold by goldsmith 3. Have hair promoting factor 4. Antifertility effects 5. Leaves used in paan masala

Uses 1. Purgatives 2. Ayurvedic medicine—for arthritis 3. Bland oil 4. Cream for sole crack

Uses 1. Strong purgatives 2. Ayurvedic medicine—for arthritis 3. For creating comedy scenes

Active principle: Abrin

Active principle: Ricin castor oil—nontoxic

Active principle: Crotin, crotonoside croton oil—highly toxic

Action Local: Irritation CVS depressant Viper bite like action4 injected

Action Local: Irritation CVS depressant Viper bite like action4 injected

Action Local: Irritation CVS depressant

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Plant and Vegetable Irritants

Fig. 9.1: Seeds of Abrus (red and pink variety)

109

Fig. 9.2: Seeds of Ricinus

Fig. 9.3: Seeds of Croton

Abrus precatorius

Ricinus communis

Croton tiglium

Fatal dose: 1–2 seeds Fatal period: 12 hrs to 3 days

6–8 seeds 12 hrs to 3 days

6–8 seeds 12 hrs to 3 days

Clinical features Clinical features 1. Local 1. Local a. At the site of injection by sui— a. At the site of injection— local severe reaction in the local severe reaction in the form of inflammation, edema, form of inflammation, swelling, oozing, necrosis with edema, swelling, oozing, evidence of hemolysis (viper necrosis with evidence of hemolysis (viper bite like). bite like)5 b. Conjunctivitis b. Conjunctivitis

Clinical features 1. Local: At the site of contact of oil to skin—erythema and blister formation

–

2. Burning pain in mouth/throat, difficulty in speech and deglutition, increase salivation, abdominal pain, nausea, vomiting, diarrhea, dizziness, dyspnea, dilatation of pupil, flushing of face, cold calmy skin, rapid pulse, fall in BP, with muscular weakness, cramps, tremor, convulsion, collapse, coma Treatment 1. Local: Wash with soap water, application of bland ointment. 2. Stomach wash 3. Demulcent 4. Supportive 5. Correction of fluids and electrolyte imbalance/ circulation2,6 6. Antiabrin2 PM findings Not specific 1. Local reaction with presence of spike/sui/sutari 2. GIT—inflamed, hemorrhagic, crushed seeds may be present 3. Organs—congested, petechial hemorrhage present

Treatment 1. Local: Wash with soap water, application of bland ointment. 2. Stomach wash with activated charcoal6 3. Demulcent 4. Supportive 5. Correction of fluids and electrolyte imbalance/ circulation2,6,7 PM findings Not specific 1. Local reaction with presence of injection mark 2. GIT—inflamed, hemorrhagic, crushed seeds may be present 3. Organs—congested, petechial hemorrhage present

Treatment 1. Local: Wash with soap water, application of bland ointment. 2. Stomach wash 3. Demulcent 4. Supportive 5. Maintenance of circulation2

PM findings Not specific 1. Local reaction at the site of contact with oil 2. GIT—inflamed, hemorrhagic, crushed seeds may be present 3. Organs—congested, petechial hemorrhage present

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Forensic Toxicology: A Comparative Approach

ML aspects

ML aspects

ML aspects

1. Suicidal: Often used 2. Homicidal: Through parentral route using sui. 3. Accidental: Children are attracted towards the seeds 4. Abortifacient 5. Arrow poison 6. Cattle poison 7. Dust used to malingerers to produce conjunctivitis

1. Suicidal: In villages 2. Homicidal: Rare, through umbrella gun7 3. Accidental: Usually in children 4. Abortifacient 5. Dust used to malingerers to produce conjunctivitis

1. Suicidal: Not common 2. Homicidal: Very rare 3. Accidental: Mistaken with castor oil 4. Abortifacient: Using oil, root 5. Arrow poison

Preparation of Sui/Sutari from Abrus precatorius seeds It is prepared by crushing the seeds of Abrus along with datura seeds and opium2,6 to make it in a powder form, from which paste is formed. Sui (needles) of size 1.5 cm × 1 cm is prepared from the paste. These suis are then dried and used to kill cattle by keeping it in front of the bamboo stick used to push cattle and also used for homicide purpose by keeping it in between the finger and then slapped over cheek or other parts of body.

Semicarpus anacardium

Calotropis

Plumbago rosea

Synonyms Marking/dhobi nut, bhela, bhilwan, biba

Synonyms: Rui Synonyms Gigantae—Akand: Purple flower Lal chitra Procera—Madar: White flower

Toxic parts All parts of plant (max. conc. in juice, seeds) Seeds: Black large heart-shaped seeds.

Toxic parts All parts of plant (max. conc. in juice, stem, leaves) Seeds: Datura like seeds with cotton fibers at one point in the spindle/crescent-shaped fruit having purple or white flowers

Uses 1. Abdominal pain 2. Ayurvedic medicines 3. Marking over the clothes (brownishyellow oily juice yields from the pericarp of seeds turns black on exposure to air,2 so used to write identification number over clothes) Active principle Semicarpol, Bhilawanol

Uses Use 1. Depilatory agent Ayurvedic medicines—quack 2. Ayurvedic medicines—by quack 3. Keeps snakes away from area. 4. Flower used for worshipping God (Lord Hanuman/Shiva)

Toxic parts All parts of plant (max. conc. in root)

Action Local: Irritation CVS depressant

Active principle Calotropin, calotoxin uscharin,2 gigantin Action Local: Irritation CVS depressant

Active principle Plumbagin Action Local: Irritation CVS depressant

Fatal dose: 6–8 seeds Fatal period: 12 hrs to 3 days

Fatal dose: Uncertain Fatal period: 12 hrs to 3 days

Fatal dose: Uncertain Fatal period: 12 hrs to 3 days

Clinical features 1. Local: Contact of juice to skin— bruise like painful lesion with marginal small blister called “Branding”, the lesion may itch and may ulcerate

Clinical features 1. Local: Contact of juice to skin—irritation of skin with blister formation which excoriates later2

Clinical features 1. Local: Contact of juice to skin— irritation of skin with blister formation which excoriates later4

Plant and Vegetable Irritants

111

2. Burning pain in mouth/throat, difficulty in speech and deglutition, increase salivation, abdominal pain, nausea, vomiting, diarrhea, dizziness, dyspnea, dilatation of pupil, flushing of face, cold calmy skin, rapid pulse, fall in BP, with muscular weakness, cramps, tremor, convulsion, collapse, coma Treatment 1. Local: Wash with soap water, application of bland ointment 2. Stomach wash 3. Demulcent 4. Supportive

Treatment 1. Local: Wash with soap water, application of bland ointment 2. Stomach wash 3. Demulcent 4. Supportive

Treatment 1. Local: Wash with soap water, application of bland ointment 2. Stomach wash 3. Demulcent 4. Supportive

PM findings: Not specific 1. Local reaction 2. GIT—inflamed, hemorrhagic, crushed seeds may be present

PM findings: Not specific 1. Local reaction 2. GIT—inflamed, hemorrhagic, crushed root may be present

3. Organs—congested, petechial hemorrhage present

PM findings: Not specific 1. Local reaction 2. GIT—inflamed, hemorrhagic, crushed leaves/stem may be present 3. Organs—congested, petechial hemorrhage present

ML aspects 1. Suicidal: Rare 2. Homicidal: Rare 3. Accidental: By mistake, quack medicine 4. Abortifacient 5. Arrow poison—not used 6. Cattle poison—not used 7. False charge2: Juice split on the body to cause injury and make a false charge of assault against enemy

ML aspects 1. Suicidal: Rare 2. Homicidal: Rare 3. Accidental: By mistake, quack medicine 4. Abortifacient: By juice 5. Arrow poison—used 6. Cattle poison—used 7. False charge: Juice split on the body to cause injury and make a false charge of assault against enemy

ML aspects 1. Suicidal: Rare 2. Homicidal: Rare 3. Accidental: By mistake, quack medicine 4. Abortifacient—by root 5. Arrow poison—not used 6. Cattle poison—used 7. False charge: Juice split on the body to cause injury and make a false charge of assault against enemy

C. gigantae Fig. 9.4: Seeds of Semicarpus

3. Organs—congested, petechial hemorrhage present

C. procera

Fig. 9.5: Flowers of Calotropis

Fig. 9.6: Roots of Plumbago

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Forensic Toxicology: A Comparative Approach

N

EW

FI

G

U

R

E

Fig. 9.7: Abrus precatorius

Fig. 9.8: Beans of Abrus with seeds

Fig. 9.9: Ricinus

Fig. 9.10:Croton tiglium

Fig. 9.11: Semicarpus

Fig. 9.12: Calotropis

Fig. 9.13: Plumbago

Plant and Vegetable Irritants

113

Fig. 9.14: Fruit of Ricinus (castor fruit)

Fig. 9.15: Fruit of Semicarpus

Capsicum annum (CHILLI) Active Principle Capsicin, capsaicin fruit, seeds and dust cause irritation

• Applied to skin/eyes—wash with water, xylocaine ointment

Signs and Symptoms • Burning, irritation, redness and swelling of mouth/throat, increase salivation, increase perspiration, watering from eyes and nose, abdominal pain, burning sensation during defecation • Death is unusual except in neonates. Treatment • When swallowed—curd, bulky food and demulcent.

(a)

Medicolegal Aspects 1. Powder is thrown in the eyes either to snatch money/articles or to escape arrest after crime 2. It is used to kill unwanted newborn baby 3. It is applied in eyes/nose/anus/vagina/ or injury to extract confession 4. It is applied in the vagina for giving punishment for infidelity 5. Hyderabadi goli: It is the paste of chilli powder used to push in the rectum for torture and confession.

(b) Figs 9.16a and b: Chilli seeds and fruit

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Forensic Toxicology: A Comparative Approach

Table 9.1: Phyto-toxicology of vegetable irritants Name

1. Aloe

2. Anacardium occidentale

3. Chrysanthemum cinerariaefolium

Synonyms: General:

Aloe vera, Ghritakumari,

Cashewnut

Pyrethrum

Bitter taste

Bitter taste.

Acrid bitter taste

Active principle:

Dried juice contains glycoside and barbaloin

Cardol present in the pericarp of the fruit

Pyrethrin I and II, Cinerin I and II present in the flowers

Clinical feature:

Abdominal pain, vomiting, diarrhea, inflammation of kidneys, kidneys increase intestinal movement and cause congestion of pelvic organs

Contact dermatitis with redness and urticaria-like lesion

Acrid bitter taste, numbness of tongue/mouth, with nausea, vomiting, diarrhea. Headache, restlessness, tremor, muscle weakness and respiratory failure.

Treatment:

Symptomatic.

• Wash the part with soap water. • Symptomatic

PM findings:

Nonspecific

Nonspecific

• Prevention of exposure. • Symptomatic. • Artificial respiration and oxygen inhalation Nonspecific

ML aspect:

• Abortifacient: Procure abortion—quackery use

• Accidental:2 to workers who collect and process the fruit for extraction of nuts • Abortifacient: Quack

• Accidental:2 Exposure and inhalation of pollen grain leading to allergic reaction. • Suicidal—unusual. • Homicidal—unusual

Name

4. Cytrullus colocynthis

5. Eucalyptus globulus

6. Pinus palustris

Synonyms:

Bitter apple, colocynth,

Nilgiri oil

Turpentine

makal, indrayan General:

–

Used in Ayurvedic medicines

–

Active principle:

Colocynthin-fruits

Cinehole—a volatile oil in stem and leaves

d and l-pinene

Clinical feature:

Abdominal pain, diarrhea (blood tinged), increase body temperature, circulatory collapse

• Dyspnea, cyanosis, excitement, ataxia, convulsion, circulatory collapse

• Abdominal pain vomiting, diarrhea. When inhaled— RT irritant. Excitement, confusion, coma, oliguria, hematuria

Treatment:

Symptomatic

• Symptomatic. • Artificial respiration and oxygen inhalation. • Maintenance of circulation

• Stomach wash. • Symptomatic

PM findings:

Nonspecific GIT—irritation Kidneys— inflammation Organs—congested

Nonspecific

Nonspecific

ML aspect:

• Accidental: By mistake.

• Accidental: Consumption of oil by mistake • Suicidal: Uncommon • Homicidal: Not possible due to the smell

• Accidental: By mistake • Suicidal: Occasionally

• Abortifacient

Plant and Vegetable Irritants

115

Table 9.2: Active principle and clinical features of other vegetable irritants Name

Synonyms

Active principle

Clinical features

1. Mangifera indica 2. Nephrolipis rosaltata 3. Narcissus

Mango Fern Daffodil

Resinous exudate Filicin Lycorine- bulb

4. Poison Oak

Sumac

–

5. Aristolocia indica

–

Aristolocin

6. Rhus toxicodendron 7. Indian Wintergreen 8. Pherulanarthex

Poison Ivy (Jav) (Asafoetida, hing)

3-pentadecyl-catechol Methyl salicylate –

9. Eugenia caryophyllus

(Cloves, lavang)

Tannin, caryophyllin

Irritation, contact dermatitis – Abdominal pain, nausea, vomiting, titanic convulsion Skin irritation causes rash and dermatitis Contact dermatitis, respiratory paralysis, hemorrhagic nephritis, GIT irritation Contact dermatitis – Digestive stimulant, psychogenic and neurogenic action –

(Hirah tutigu)

Colchicine

–

10. Colchicum leutium

Table 9.3: Toxic substance and active principles in poisonous plants4–6, 8 Toxic substance Toxalbumin

Glycosides

Alkaloids

Glucoside Resins Juice/oils Plant acid

Active principles Abrin Ricin Crotin Curcin Calotropin, calotoxin Crotonoside Plumbagin Cerberin, thevetin, thevotoxin Nerin, oleandrin Digoxin, digitalin Capsaisin Atropine, hyoscine Aconitine Nicotine, nicotianin

Plants Abrus precatorius Ricinus communis Croton tiglium Jatropha curcas Calotropis Croton tiglium Plumbago rosea Cerbera thevetia/odallam Nerium odorum Digitalis purpura Capsicum annum Datura Aconitum ferox/napellus Nicotiana tabacum

Type of poison Vegetable irritant Vegetable irritant Vegetable irritant Vegetable irritant Vegetable irritant Vegetable irritant Vegetable irritant Cardiac poison Cardiac poison Cardiac poison Vegetable irritant Deliriant Cardiac poison Cardiac poison

Strychnine, brucin Curarine

Strychnos nux vomica Chondrodendron tomentosum (Curare) Papaver somniferum Erythroxylum coca Conium maculatum Argemone mexicana Abrus precatorius Cannabis sativa Semicarpus annacardium Spinach

Spinal poison Peripheral nerve poison Somniferous poison Deliriant poison Peripheral poison Food poisoning Vegetable irritant Deliriant poison Vegetable irritant –

Morphine, codeine, thebaine Cocaine Conine Berberine, protopine Abralin Cannabinol (THC) Semicarpol, bhilawanol Oxalic acid

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IMPORTANT QUESTIONS

1. Enumerate vegetable irritants with their uses. Describe clinical manifestation, treatment and medicolegal aspects in case of consumption of seeds of Abrus precatorius. Add a note on preparation of sui from these seeds. 2. What is the difference in the seeds of crotin and castor? Write clinical features and management of their poisoning. 3. Enumerate roadside poisons. Write clinical features and medicolegal importance of poisoning with Semicarpus anacardium. 4. Enumerate active principle of any four vegetable irritants. Write clinical feature, treatment and medicolegal aspect of Calotropis poisoning. 5. Write difference between seeds of datura and capsicum. Write medicolegal aspect of chilli powder. Describe the fruit of datura and castor. SPECIFIC LEARNING OBJECTIVES

After reading this chapter, the reader should be able to: • Classify poisonous plants with their examples • Enumerate different vegetable irritants • Enlist toxic parts, uses, fatal dose, fatal period and active principle of different vegetable irritants • Explain clinical features, treatment, postmortem findings and medicolegal aspect of different vegetable irritant poisoning

• Define toxalbumin with examples and describe the method for preparation of needles (sui) from Abrus precatorius seeds. • Enlist different toxic substances and principles in poisonous plants References 1. Phytotoxicology. https://www. britannica. com/ science/phytotoxicology. Plant poisons (Phytotoxins). https://www.britannica.com/science/poisonbiochemistry/Types-of-poison#ref28140. Assessed on 2/12/2018. 2. Nandy A. Principles of Forensic Medicine. New Central Book Agency (P) Ltd: Calcutta, 2nd edn Reprint, 2004: 498–505. 3. Singhal SK. Singhal’s Toxicology at a glance. 9th edn, National book depot: Mumbai.2016: 66– 71. 4. Dikshit PC. Textbook of Forensic Medicine and Toxicology. 2nd edn, PEEPEE Publisher and Distributors (P) Ltd. New Delhi. 2014: 501–8. 5. Bardale R. Principles of Forensic Medicine and Toxicology. 1st edn, Jaypee Brothers Medical Publishers (P) Ltd: New Delhi. 2011: 467–76. 6. Pillay VV. Textbook of Forensic Medicine and Toxicology. Paras Medical Publisher: Hyderabad, 17th edn, 2016: 538–49. 7. Rashmi Aggarwal, Hemant Aggarwal, Pradeep Kumar Chugh. Medical management of ricin poisoning. Journal of Medical & Allied Sciences. 2017; 7(2): 82–6. 8. Reddy KSN, Murthy OP. The Essential of Forensic Medicine and Toxicology. 32nd edn, Om Sai Graphics: Hyderabad. 2013:503–97.

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10 Animal Irritants Animal irritants include snakes, scorpions, bees, wasps, cantharides, spider, etc. which cause venomous bite or stings. Envenomation1 is the process by which venom is injected by the bite or sting of a venomous animal. Venom refers to injection of toxin through bite or sting. Poison refers to toxin that has to be ingested or swallowed for causing deleterious effect. Snakes may be venomous and non-venomous. But still poisonous and non-poisonous snakes have been commonly referred in practice. It has been estimated that five million snakebite cases occur worldwide every year, causing about 100,000 deaths. In India, nearly 200,000 fall prey to snakebite per year and 35,000–50,000 of them die every year.2

SNAKES (OPHIDIA)

Snakes belong to class reptilia, order squamata and suborder serpentes. Snakes are found all over the world except Antarctica region and in Ireland, Iceland and New Zealand.3 In the world, there are about 3000 species of snakes, 600 are venomous4 (WHO) and only half of these are capable of inflicting a lethal bite. India has over 250 species of snakes out of which about 50 species are venomous.5 The common poisonous snakes in India are Cobra, Krait, Russell’s viper, Saw-scaled viper and Sea snakes. Deaths due to snakebites are mainly accidental in nature. GENERAL CHARACTERISTICS

1. Snakes have an elongated body and a short tail that is the part behind vent, and has no limbs. Vent is an opening in the rear part of the body for intestine and genitourinary system. 2. The body is covered with scales. 3. On the head, there are 2 eyes, 2 nostrils, but no external ear. 4. Tongue is forked and serves as a sense organ. 5. They are cold blooded creatures with carnivorous habits. They use sharp teeth 117

and strong muscles to catch the prey. The mouth is easily distensible allowing it to swallow even large animals as a whole. 6. Teeth are thin, directed backwards and the upper marginal teeth are modified and are known as fangs. Fangs can be replaced in 3–6 weeks when broken. The fangs are solid in non-poisonous and grooved/canalized in poisonous snakes for transport of venom from the poison glands, i.e. modified parotid salivary glands, to which they are connected through ducts. 7. In poisonous snakes, parotid glands are situated below and behind the eyes, one on each side secreting toxic saliva and acts as poison glands. Fangs of elapids/sea snakes are short, fixed and grooved, and that of vipers are long, movable and canalized. 8. During the process of bite, the glands are pressed and venom is squeezed and channeled through the grooves or canal of the fangs. 9. Some are viviparous (gives birth to young ones in vipers) and some are oviparous (lays eggs, e.g. cobra, pythons, water snakes).

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Classification of Snakes On the Basis of their Families6 1. Colubridae: African boomslang, twig snake 2. Elapidae: Cobra and krait (commonly called elapids), coral snakes, all Australian venomous snakes. 3. Hydrophiidae: Sea snakes. 4. Viperidae: Vipers 5. Atractaspididae: Mole vipers or adders. On the Basis of Venom

1. Elapids—neurotoxic 2. Vipers—vasculotoxic 3. Sea snakes—myotoxic

4. Banded kukri 5. Sand boa The non-poisonous snakes, which may resemble poisonous snake are as follows: Non-poisonous snakes

Poisonous snakes

Rat snake Common cat Banded kukri Sand boa Common wolf

Common cobra Saw-scaled viper Banded krait Russell’s viper Common krait

Snakes may be:

1. Poisonous/venomous 2. Non poisonous/non-venomous Common Poisonous Snakes in India 1. Cobra: King/common cobra (Table 10.2) 2. Krait: Common/banded 3. Viper: Pit/Russell’s/Saw-scaled 4. Sea snakes: Banded sea snakes, amphibian sea snakes Common Non-poisonous Snakes in India7 1. Rat snake (Dhaman) 2. Vine snake 3. Bronze back tree snake

Poisonous Non-poisonous Fig. 10.1: Belly scales

Differences Between Poisonous and Nonpoisonous Snakes Table 10.1 shows the differentiating features between poisonous and non-poisonous snakes.

Table 10.1: Differences between poisonous and non-poisonous snakes Features

Poisonous snakes

Non-poisonous snakes

1. Belly scales: Size (Fig. 10.1) Distribution 2. Head: Size Scales (Fig. 10.2) 3. Teeth

Large Cover entire breadth Usually small (pit, cobra, krait) Usually small except cobras At least one pair of teeth in upper jaw is modified to form fangs Present and canalized/grooved Abruptly tapering tail, rounded Usually nocturnal Stout, dull colour Usually two fang marks present

Small Never cover entire breadth Usually large Usually large All teeth are uniformly small, attached to short maxillary bone

4. Fangs 5. Tails 6. Habits 7. Physical features 8. Bite marks (Fig. 10.18)

Absent Gradually tapering long tail May be nocturnal or diurnal Slender, bright-coloured Semicircular set of teeth mark present

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Table 10.2: Differences between king cobra and common cobra Common cobra

King cobra

5–6 feet length

8–18 feet length

Black, brown or cream color

Usually jet black color

Habitat near human dwelling

Found in hills and dense forest

Spectacle mark present on hood

No spectacle mark on hood

Features of Poisonous Snakes in India [Tables 10.4 and 10.5] 1. Cobra: It is usually black of about 5–6 feet. It has a hood with one or two spectacle marks on its dorsal surface. The third supralabial is large and touches the eye. It prefers barren land near human habitate. 2. King-cobra: It is usually jet black color of about 6–18 feet. It has a hood without having any mark. It prefers dense forests. 3. Common Krait: It is usually steel-black, 3–5 feet. There are four infralabial shields on head of which 4th is largest. The central rows of scales on back are large and hexagonal. It prefers agricultural area and near the houses. 4. Banded krait: It is 5–7 feet and has alternate black and yellow bands on the body. 5. Pit viper: It is usually green or yellow of about 1–3 feet. It has a green pit between eye and nostril. It is found in hills. 6. Russell's viper: It is usually light brown of about 4–5 feet. Head is triangular and

Poisonous

Non-poisonous

Fig. 10.2: Head scales

has white V-shaped mark with its apex pointing forwards. 7. Saw-scaled viper or echis carinata: It is usually brown of about 1–1.5 feet. Head is triangular with white mark resembling an arrow or foot of a bird. The ridges in the middle of each scale are like a saw, hence the name saw-scaled viper.

Fig. 10.3: King-cobra (no spectacle mark on hood)

Table 10.3: Differences between cobras and vipers Features

Cobras

Vipers

1. Body 2. Head

Long and cylindrical Small with hood seldom broader than body Same width as neck Has 2 fangs (~4–6 mm) and other teeth Short, fixed, grooved Neurotoxic Round pupil Round Oviparous

Short and stout Large and triangular Broader than body Wider than neck Has only 2 fangs (12–15 mm) Long, movable, canalized Hemotoxic (vasculotoxic) Vertical pupil Tapered Viviparous

3. Upper jaw 4. Fangs 5. Venom 6. Eyes 7. Tail 8. Parity

5–6 feet

Usually black or cream to black to brown

Flat with hood present with one or two dark round spots surrounded by an eclipse c/s ‘spectacle mark’ on dorsal aspect

Head scales are large with 3rd supralabial touches the eye and nasal shields Round

• Ventral aspect of hood bears • Ventral aspect of hood bears • Ventral aspect of mouth has 3 dark bands on central part 3 dark bands on central part and only 4 infralabials and and a white band in an area a white band in an area where 4th infralabial is the largest where hood touches the hood touches the body body • Tiny triangular shield • Tiny triangular shield between between 4th and 5th 4th and 5th infralabial shield infralabial shield

Cover the entire width

Scales are entirely present proximally but divided in the distal ends

Length

Colour

Head shape and mark

Head scales

Ventral aspect of mouth

Belly scales

Tail

Neurotoxin

15 mg

20 mins to 6 hours

Toxin

Fatal dose

Fatal period

Pupils

All over India, Sri Lanka, Burma

20 mins to 6 hours

15 mg

Neurotoxin

Scales are entirely present proximally but divided in the distal ends

Cover the entire width

Head scales are large with 3rd supralabial touches the eye and nasal shields Round

Flat with hood present with no ‘spectacle mark’on dorsal aspect

Usually jet black or brownish black, greenish, yellow

8–18 feet

Hills and forest of S. India, Odisha, Assam, Himalaya

20 mins to 6 hours

1 mg

Neurotoxin

Scales are entirely present and not divided

Cover the entire width

Round

Head scales are small

Oval with one enlarged central row of hexagonal scales on dorsal aspect

Usually steel black with single or double narrow band across their back all over up to tip of tail

3–5 feet

All over India, and near dwelling house

Maniyar (Maharashtra), Kawariya (Punj.), Chitti (Cal.), Kalotaro (Guj)

Found in

NagRaja, Daras

Nag, Gokhurra

Common krait

Synonyms

King-cobra

Common cobra

Table 10.4: Characteristic features of common poisonous snakes in India—Cobra and Krait

Snakes

20 mins to 6 hours

10 mg

Neurotoxin

Scales are entirely present and not divided

Cover the entire width

• Ventral aspect of mouth has only 4 infralabials and 4th infralabial is the largest

Head scales are small with black mark on its neck spreading up to the eyes Round

Oval with one enlarged central row of hexagonal scales on dorsal aspect

Alternate jet black and yellow bands across its back

5–7 feet

–

–

Banded krait

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Animal Irritants

121

Fig. 10.4: Common cobra with spectacle mark

Fig. 10.5: Common krait (Courtesy: Shrikant Uike)

Fig 10.6: Banded krait (Courtesy: Shrikant Uike)

Fig. 10.7: Cobra head scales—large scales and 3rd labial touches the eye and nasal shields

Fig. 10.8: Krait head—4th infralabial is largest (view from below)

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Fig. 10.9: Russell’s viper (Courtesy : Shrikant Uike)

SNAKE VENOM

It is the toxic saliva secreted by the specialized salivary glands. The snake venom on ingestion is non-poisonous since it can be digested. Envenomation (poisoning) occurs only due to direct snakebite or when the venom is injected or on contact with injured skin/ mucosa.8 Features 1. Physical: Clear, transparent, pale liquid when fresh. It becomes yellowish, opaque, granular powder on drying and remains active for many years. 2. Chemical: It is a heterogeneous mixture of proteins in the form of enzymes, peptides and polypeptides. 3. Enzymes: The constituents of different snakes venoms are proteinases, hydrolases, transaminase, hyaluronidase, phos-

Fig. 10.10: Saw-scaled viper

pholipase A, B, C and D, ribonuclease, deoxyribonuclease, phosphomonoesterase, phosphodiesterases, 5-nucleotidase, ATPase, alkaline phosphatase, acid phosphatase, cholinesterases, coagulases, agglutinins, fibrinolysin, hemolysin, etc. 4. Types of venoms and action • Elapids: Neurotoxin. It blocks the neuromuscular junction.9 Neurotoxic features are similar to d-tubocurarine leading to flaccidity of muscles. However, Cobra venom is almost 15–40 times more potent than tubocurarine. • Vipers: Hemolytic and hemotoxic. It causes intravascular hemolysis and depression of coagulation mechanism and leads to hemorrhage and necrosis. • Sea snake: Myotoxic. It leads to muscle pain, myoglobinuria and hyperkalemia.9

Hilly area 2–4 feet Usually green or yellow with pit between eye and nostril Triangular, heavy with deep depression ‘pit’ on each side between eye and nostril Smaller Vertical Flat and broad

– Cover the entire width Scales are divided throughout Vasculotoxic 100 mg 2–4 days

Synonyms

Found in Length

Colour

Head shape and mark

Head scales

Pupils

Body

Other peculiar

Belly scales

Tail

Toxin

Fatal dose

Fatal period

Cobra: Scales are divided distally

Pit viper –

Snakes

Viper: Scales are divided throughout the tail

Tail of poisonous snakes

2–4 days

40 mg

Vasculotoxic

Scales are divided throughout

Cover the entire width and broad

Snake produces terrible hissing sound when about to attack

Roundish, smooth

Vertical

Smaller

Triangular, heavy with white V-shaped mark with its apex pointing forward

Buff or light brown and pitless with 3 longitudinal regular chain-like pattern or rows on the back

Throughout India in the plains 4–5 feet, heavy body with narrow neck

Ghonus (Marathi), Kander (Hindi), Chital (Gujarati), Daboia

Russell viper

Table 10.5: Characteristic features of common poisonous snakes in India —Vipers

Krait: Scales are not divided

2–4 days

8 mg

Vasculotoxic

Scales are divided throughout

Cover the entire width and broad

Snakes produce peculiar rustling sound while moving

Broad and rough having serrated ridge and continuous wavy line along each flank of the back

Vertical

Smaller

Triangular, heavy with white mark resembling a bird’s footprint or an arrow

Brownish or brownish grey

– 1–1.5 feet

Phoorsa

Saw-scaled viper

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Fig. 10.11: Pit viper

Fig. 10.14: Dorsal aspect of hood of common cobra

Fig. 10.12: Belcher’s sea snake

Fig. 10.13: Poisonous snake: Viper-Belly scales complete and tail scales are divided throughout

Fig. 10.15: Ventral aspect of hood of common cobra

Animal Irritants

Fig. 10.17: Fangs of viper

Fig. 10.16: Fangs of cobra

5. The action of different constituents of snake venom is as follows: • Hyaluronidase: Spread venom. • Hemolysin: Lysis of RBC. • Phospholipase: Hemolysis. • Proteases: Dissolution of blood vessels. • Proteolytic enzymes: Digestion and destruction of tissue proteins. • Leukolysin: Lysis of WBC. • Cytolysin: Damage of internal viscera. • Rhabdomyolysin: Necrosis of muscles. • Fibrinolysin: Breakdown of fibrin/clot. 6. Absorption: 10–12 The neurotoxins of elapids and sea snakes are absorbed rapidly into the bloodstream (therefore causing rapid systemic effects), whereas the much larger molecules of viper venom are taken up more slowly through the lymphatics (causing severe local effects). Most venoms do not cross blood–brain barrier.

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7. Fatal dose, fatal period and amount of venom injected per bite:13 Snakes

Fatal dose (of dried venom)

Amount injected per bite

Cobra

12–15 mg

200–250 mg

Krait

5–6 mg

20–25 mg

Russell’s viper

15–20 mg

150–200 mg

Saw-scaled viper 8 mg

5 mg

Fatal period Colubridae: 1/2 hr to 24 hr. Viperidae: 1 to 4 days. CLINICAL FEATURES OF NON-POISONOUS SNAKEBITES

• Fear and apprehension; sweating. • Feeble pulse, hypotension, syncope, rapid and shallow breathing. • Bite area may show multiple teeth marks.

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SIGNS AND SYMPTOMS OF POISONOUS SNAKEBITES 1. Psychological trauma: Fright is the most common symptom following snakebite due to enhanced systemic absorption of venom. It develops almost rapidly and may produce psychological shock and cause sudden death. Fear may cause transient pallor, sweating and vomiting 2. Dry bites: In at least 20% of pit viper bites and a greater percentage of elapid and sea snakebites, no venom is injected.12 3. Local manifestations are present in the form of one or more fang (bite) marks seen as punctured wound. Local features are more prominent in vipers as compared to elapids bites. a. Elapids: There is burning with triple response (i.e. redness, swelling, and inflammation) at the site of bite. Thus, there is mild pain with local swelling and blistering. In Krait, usually do not have any local reaction.12 b. Vipers: Intense pain with radiation and tenderness followed by edema, swelling, cyanosis, oozing of blood, ecchymosis, hemorrhagic bullae and serum-filled vesicles/ blisters,6 cellulitis and sometimes significant tissue loss with features of necrosis/gangrene.13 If there is no swelling 2 hours after a viper bite, it is safe to assume that there has been no envenoming.14 c. Sea snakes: The bite is painful but soon becomes painless. It takes 2 hours to produce signs. Secondary infection may occur due to bacterial flora in the oral cavity of the snakes.15 4. General features: There is flushing, dyspnea, palpitation, sweating, and tightness in chest due to sympathetic overactivity. Apart from these, in elapids bites, there may be vomiting, hypersalivation, blurring of vision and ‘gooseflesh’.12 In Krait, the bite may be unnoticed as it occurs usually at night. The patient wakes up with vomiting and cramping abdominal pain followed by diarrhea12 (predominantly ANS involvement). Sea snake envenomation causes headache, a thick feeling of the tongue, thirst, sweating and vomiting.12 5. Systemic manifestation:6, 12 Systemic manifestation depends upon the type of venom predominantly present like neurotoxic (cobras and kraits), hemorrhagic (vipers) and myotoxic (sea snakes). a. Elapids: Neurotoxicity: In elapids, paralysis is first detectable as ptosis and external ophthalmoplegia appearing within 15 min of bite along with difficulty in speech and deglutition, salivation and frothing from mouth. This is followed by respiratory paralysis, muscle weakness and pain, staggering, spreading paralysis (ascending from lower limbs), convulsions and death. With Krait bite, the s/s is less rapid and there is no convulsion, nausea and frothing but there is more drowsiness. Cardiotoxicity: Cause direct myocardial damage leading to arrhythmias, tachy/bradycardia, hypotension. b. Vipers: Clotting defects and hemolysis: Hemostatic abnormalities are characteristic of envenoming by viperidae. Bleeding from multiple sites including gums, nose, GIT (hematemesis, malena), urinary tract, injection sites, skin (multiple petechiae and purpura), conjunctivae, and internal organs particularly kidneys. There is intravascular hemolysis leading to hemoglobinuria and hypotension and intracranial hemorrhage. Nephrotoxicity: Renal failure secondary to ischemia. Shock: Due to fright and hypovolemia, and hemorrhage into adrenals/pituitary. c. Sea snakes: Myotoxicity: Myotoxin causes myalgia, myopathy and rhabdomyolysis (leading to myoglobinuria— due to muscle necrosis), vomiting, collapse, muscular pain, muscle stiffness, hyperkalemia (increased K+) and increased serum transaminase levels.

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Table 10.6: Difference in clinical manifestation of colubrine bite and viperine bite Features 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11.

Colubrine bite (cobra) (Neurotoxicity)

Viperine bite (viper) (Hemotoxicity)

Onset of symptoms Early—within 5–10 min Feeling of intoxication Marked Drooping of eyelids (ptosis) Present Involvement of tongue/larynx Paralyzed Salivation Drooling of saliva from mouth Speech and deglutition Lost Pupils Normal Gait Staggering Blood coagulability Not affected Hemorrhagic features Not present or less marked Death Due to respiratory paralysis

12. Development of gangrene

Early, wet type

DIAGNOSIS OF SNAKEBITE POISONING [IN OPHITOXEMIA—POISONING BY SNAKE VENOM)

Diagnosis depends on 1. Fang marks: Usually two fang marks are seen in the form of punctured wound, separated from each other by about 1 to 4 cm. 2. Identification of snakes: Refer to Tables 10.4 and 10.5. 3. Laboratory methods: Lab diagnosis is poor but are useful for monitoring, prognosis and determining stages of intervention: a. Blood changes: Like anemia, leukocytosis and thrombocytopenia and hypofibrinogenemia. b. Peripheral smear: Shows evidence of hemolysis, particularly in viperine bites. c. Deranged coagulant activity: Prolonged clotting time and prothrombin time. d. Immunodiagnosis: Consists of: i. ELISA: To identify the species based on antigens in the venom. These tests are expensive and not freely available and hence are of limited value. ii. Radioimmunoassay (RIA). iii. Immunodiffusion. iv. Countercurrent immunoelectrophoresis.

Longer—within 10–20 min Not marked Not observed No effect Absent No effect Dilated, not reacting to light Not so, but s/o general paralysis Completely deranged Most important feature Pulmonary thrombosis or toxic action on heart, blood, kidneys. Slow, dry type

4. Metabolic changes: Like hyperkalemia and hypoxemia with respiratory acidosis, especially with neuroparalysis. 5. Urine changes: Hematuria, proteinuria, hemoglobinuria or myoglobinuria.

Fig. 10.18: Fang marks of snakes

TREATMENT

In non-poisonous snakes a. Allay fear and anxiety. b. Console patient that not all snakes are poisonous. In poisonous snakes, treatment includes a. Field management b. Hospital management

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Fig. 10.19: General manifestations of snakebite

A. FIELD MANAGEMENT

1. To allay fear and anxiety: First step in snakebite treatment is to allay fear and anxiety, which is the commonest cause of mortality in snakebite. The patient should be reassured that every snake is not poisonous. Patient should be taken to hospital at the earliest for management. 2. Washing the area of bite: Bite area should not be washed as rubbing or touching the area will help the venom to spread more rapidly. Moreover, traces of venom that are left on the skin can be used to identify the snakes (where such facilities are available) and type of anti-venom that should be used. 3. Avoid incision and sucking:6 There is no benefit in cutting or sucking the bite as the venom is deeply injected and or absorbed. Rather avoid incising or cooling bite site, as neurotoxin may be rapidly absorbed through it.

4. Pressure immobilization technique: Immobilization is the most effective first aid. It greatly restricts absorption and circulation of these venoms (particularly neurotoxic in elapids/sea snakebites6) which tends to cause lesser local tissue effects than viper bites. It prevents spread of venom and relieves pain. Apply firm bandage/broad tourniquet proximal to the site of bite (if on extremity, preferably on a single bone) to minimise the spread of the venom. The pressure of torniquet should be tight enough to occlude the lymphatics and venous flow but not the arterial flow,12 so as to permit a finger to slip under it. The tourniquet should be released for 20–30 sec. every 15 min to avoid gangrene. In viper bite, the torniquet should not be applied as the procoagulant enzymes present in viper venom cause the blood to clot. When such torniquet is released, the

Animal Irritants

clot will rapidly enter the circulation and cause embolism and death.13 Moreover, application of bandages/tourniquet to limit venom spread is ineffective and may cause greater local tissue damage, particularly due to necrotic venom.6 B. HOSPITAL MANAGEMENT6

Victim should be closely monitored while a history is obtained quickly and rapid through physical examination is performed. • Evaluation of progression of local envenomation by marking the level of swelling in the bitten extremity every 15 minutes (after positioned the limb at ~ heart level and release of tourniquet). • Evaluation of local and systemic hemorrhage by hypotension. • Evaluate the degree of hemolysis/ thrombocytopenia/renal or hepatic function by whole blood clotting time (for 20 min12) and urine testing for blood or myoglobin, every 6 hourly until clinical stability is achieved. 1. Fluid resuscitation with isotonic saline (20–40 ml/kg IV) should be initiated if there is any evidence of hemodynamic instability. If fail to respond, then 5% albumin (10–20 ml/kg) may be given. 2. Antivenom administration 3. Vasopressor (e.g. dopamine) should be added. 4. Tetanus immunization 5. Prophylactic antibiotics 6. Pain control with acetaminophen or narcotic analgesic. 7. Wound care once coagulation has been restored. 8. Neurotoxicity from the elapid bites may be harder to reverse with antivenom and further doses of antivenom is not beneficial. In such cases, victim may be maintained on mechanical ventilator until recovery (takes days or weeks).6 • Patient with clear evidence of neurotoxicity after snakebite (e.g. ptosis) should receive: a. Pretreatment with atropines—0.6 mg IV (children—0.02 mg/kg)

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b. Acetylcholinesterase inhibitors like Edrophonium—10 mg IV (children – 0.2 mg/kg) OR Neostigmine—1.5– 2 mg IM (children 0.025–0.08 mg/kg) • If improvement is evident within 5 min, then continue neostigmine 0.5 mg IV/SC every 30 minutes as needed along with continuous IV infusion of atropine over 8 hours. Neostigmine is given to prevent respiratory paralysis.16 • Maintain airway with endotracheal intubation, if required. Specific Therapy: Antivenom Serum or Antivenene Preparation: It is prepared by injecting the snake venom into horse and extracting the antibodies in the serum. Antivenoms or Antivenins may be monovalent (species specific, not available in India) or polyvalent (effective against cobra, krait, pitless viper). This serum is freeze dried (lyophilised) and is available as granular powder. It is reconstituted by adding 10 ml of diluents supplied along with serum. Indications:6 Antisnake venom (ASV) should be used cautiously because of its hypersensitivity reactions, but should be given irrespective of the sensitivity. 1. For Viperids bites and cytotoxic elapids: Any evidence of systemic envenomation ( like coma, hypotension, shock, bleeding, DIC, ARF, etc. and laboratory abnormalities) and significant progressive local findings (swelling crossing a joint or involving more than half the affected limb). 2. For neurotoxic elapids: First sign of any e/o neurotoxicity (like ptosis-cranial nerve dysfunction) or peripheral neuropathy. Dose: Firstly, sensitivity test is done (if time and condition of the patient permits) by giving 0.1 ml reconstituted serum intradermally on one forearm. Control with 0.1 ml saline in opposite forearm. • lf a person is sensitive, i.e. +ve test (appearance of erythema or wheal > 10 mm within 30 minutes), then desensitise with 0.01 ml of 1:100 solution and increase the

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concentration gradually at intervals of 15 minutes, till 1.0 ml SC can be given 2 hourly; under cover of adrenaline, antihistaminic, and corticosteroids. Some recommended6 pretreatment with IV antihistamines (e.g. diphenhydramine, 1 mg/kg to a maximum of 100 mg and cimetidine, 5–10 mg/kg) or even epinephrine (0.01 mg/kg IM up to 0.3 mg) or glucocorticoids (for serum sickness) like oral prednisone 1–2 mg/kg daily until all findings resolve and then tapered over 1–2 weeks. • If not sensitive, conventionally: a. For elapid (neurotoxic) bite—100 ml ASV (10 vials) dissolved in DNS/normal saline in IV drip for 1 hour, followed by 100 ml ASV slowly over 6 hours b. For viper (hemotoxic) bite—100 ml ASV (10 vials) dissolved in DNS/ normal saline in IV drip for 1 hour. Then after 6 hours, whole blood clotting time is done. If clotting time is more than 20 min, then 50 ml ASV is repeated; and if less than 20 minutes, then there is no need of further dose. The antivenom should be continued until the victim shows definite improvement like stabilized vital signs, reduced pain and restored coagulation.6 Types a. Polyvalent Antisnake Venom Serum 17 (ASV serum—prepared in Haffkine’s Institute, Bombay) is given 20 ml IV prepared by dissolving powdered serum in distilled water, administered at the earliest, but may be helpful even after 6–7 days after bite. It is repeated at 1–6 hourly interval till symptoms of envenomation disappear (up to 300 ml in viper bites and more in cobra).17 Local injection is useful in vipers to avoid local gangrene.17 b. Polyvalent a ntivenene (prepared at Kasauli) may be used as a substitute, if ASV serum is not available or patient is very sensitive. Despite widespread use of antivenom, there are virtually no clinical trials to determine the ideal dose.

PM FINDINGS

a. Colubrine Snakebite • Two puncture marks of fangs: ½ inch deep with oozing of serum and blister and necrosis at the site of bite (Figs 10.20 and 10.21). • Blood is fluid with dark red color. • Froth in mouth/nostrils. • Signs of asphyxia present. • Histology:13 Nervous tissue shows changes in Nissl’s granules, fragmentation and swelling of nuclei. Cells of medulla show acute granular degeneration. b. Viperine Snakebite • Two puncture marks of fangs: 1 inch deep with oozing of fluid blood and swelling, inflammation, discolouration, extravasation of blood or cellulites. On cut section underlying soft tissue edema, hemorrhage and oozing of fluid blood present (marked local features) (Figs 10.22 and 10.23). • Blood is fluid with dark red color. • Evidence of hemorrhage in GIT, RT, UT and petechial hemorrhage in pleura, pericardium, lungs, and kidneys. Hemorrhage present over endocardium, IV septum, papillary muscle. • Visceral organs are congested. MEDICOLEGAL ASPECTS

1. Accidental: Snakebite is usually accidental.18 Annually about 2 lakh people are bitten by snakes and 50,000 die.2 It is also seen in snake charmers. 2. Suicidal: Rarely except by Cleopatra.19 3. Homicidal: Rarely and mostly by indirect method or for giving punishment in ancient period. One case of contract killing by direct snakebite has also been reported.8 4. Cattle poisoning by placing snakes and banana in an earthen pot and irritating snakes by firing it. The cobra bites the banana. Fruit is then taken out and smeared into a rag to be injected into rectum of the animal by bamboo stick.

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Fig. 10.20: Cobra bite mark

Fig. 10.21: Hemorrhage on cut section

Fig. 10.22: Viper bite marks

Fig. 10.23: Extensive hemorrhage on cut section

CANTHARIDES (SPANISH FLY—NOT SEEN IN INDIA)

SCORPIONS

It is an insect about 1.5 cm long, shining greenish in appearance18

Scorpions are long, fleshy, five segmented, eight legged, and have a tail. The end part of the tail has two poison glands and a sting. The scorpion when agitated injects the venom by pressing its sting leaving behind the broken tip of sting in the tissue on the body of victim.18 Color varies from light yellow to black.

Uses 1. As counterirritant and in other medicinal preparation 2. Aphrodisiac Active principle—cantheridin

– Active principle—scorpion venom is a toxalbumin (a proteinous substance) consist of neurotoxin and hemolysin

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Action:18 • Locally—irritant • Systemic—nephrotoxic

Action: • Locally—irritant • Systemic—neurotoxic and hematotoxic actions

Fatal dose: 30 mg cantheridin Fatal dose: 12–24 hrs

Fatal dose: Uncertain Fatal period: Uncertain

Clinical features18 1. Local application to skin causes burning pain, redness and vesiculation/blister formation 2. On ingestion—burning pain in throat, abdominal pain, vomiting, blood tinged mucus stool and straining during motion followed by renal failure, CV collapse, convulsion, coma, death. 3. Urine—scanty containing blood, albumin

Clinical features 1. Local manifestations—(more severe than snakes)— bite is usually associated with little swelling, severe pain, paresthesia and hyperesthesia, accentuated by tapping on the affected area (tap test).6 2. Systemic manifestations—nausea, vomiting, restlessness, blurred vision, convulsions, cyanosis with perspiration, salivation, and nasal secretion, slurred speech. 3. Small quantity of the venom is injected—hence mortality is negligible

Treatment 1. Restriction of fat as it dissolves cantheridin and helps absorption 2. Stomach wash 3. Plenty of water to drink 4. Demulcent drinks 5. Symptomatic

Treatment 1. Immobilization and application of tourniquet proximal to bite 2. Wash the wound with water or KMnO4 3. Ice packs, analgesic and antihistaminics6 4. Anti-inflammatory. 5. Local infiltration of anaesthetics to lessen pain. 6. Antivenin.6,18 7. IV calcium gluconate to control swelling 8. IV glucose, saline and hydrocortisone

PM findings PM findings • S/o irritation in mouth/esophagus/stomach • Local: At site of scorpion bite—swelling, edema, • Stomach: Wall—swollen; Mucosa—hemorrhagic; underlying tissue haemorrhagic Contains—particles of exoskeleton of insect • Visceral organs congested • Visceral organs—congested with hemorrhagic spots present • Urinary bladder—reddish urine due to hemorrhagic mucosa. Kidneys—hemorrhagic Medicolegal aspects 1. Accidental: During medicinal use for counterirritant or for aphrodisiac use 2. Suicidal/homicidal: Rare 3. Abortifacient 4. Aphrodisiac: To increase sexual desire

Medicolegal aspects 1. Poisoning is accidental 2. Spraying DDT kills scorpions

BEES

WASPS, HORNET

It causes manifestation by stinging

It causes manifestation by stinging

Venom 1. Biogenic amines: Histamine, 5-hydroxytryptamine, acetylcholine 2. Enzymes: Phospholipase A, hyaluronidase, cardiotoxin 3. Toxic peptides: Mellitin, apamin, mast cell degranulating peptides

Venom 1. Biogenic amines: Histamine, 5-hydroxytryptamin, acetylcholine 2. Enzymes: Phospholipase A, hyaluronidase, cardiotoxin 3. Toxic peptides/other: Kinin/antigen-5, acid phosphatase

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Clinical features Local: Stinging causes local pain, redness, swelling Systemic effect: S/o collapse with sweating, fall of BP, nausea, vomiting, bronchospasm, tingling sensation, flushing, dizziness, syncope, urticaria, glottis edema, angioedema, renal failure, hemolysis with hematoglobinuria Treatment 1. Remove honeybee/wasps sting embedded in the skin. 2. Wash the bite site with bicarbonate in bee sting and with vinegar in wasp’s sting followed by application of ice packs to reduce spread. 3. Elevation of affected site with administration of analgesic, antihistaminic and local calamine cream. 4. Epinephrine HCl: 0.3 mg SC for anaphylaxis 5. Glucocorticoids IM in severe reaction6 6. Artificial respiration + O2 inhalation. 7. Antihistaminic cream locally ML aspect: It is almost always accidental

ML aspect: It is almost always accidental

BLACK SPIDER

BROWN SPIDER

RED ANTS

Black spider bite is toxic

Bite inject hemolysin and norepinephrine18

Red ants bite injects alkaloid, solenopsin A (has hemolytic and phytotoxic actions)18

Clinical manifestation 1. Local: Painful ulceration at the site of bite 2. Systemic: Nausea, vomiting, fever, hematuria, albuminuria, arthralgia18

Clinical manifestation 1. Local: Urticarial lesion followed by pustulation 2. Systemic: Increased BP, retrosternal pain, respiratory difficulty18

Clinical manifestation 1. Local: Pain and cramps which extends upward 2. Systemic: Increase BP, nausea, vomiting, respiratory difficulty

Treatment Treatment 1. Sedatives 1. Symptomatic 2. Ca gluconate 3. Neostigmine + atropine sulphate (0.5 mg each) 4. Curariform drug

Treatment 1. Adrenaline 2. Antihistaminic

ML aspect: Accidental

ML aspect: Accidental

Fig. 10.24: Honeybee

ML aspect: Accidental

Fig. 10.25: Wasps

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Fig. 10.26: Giant Indian hornet

VENOMOUS AQUATIC ANIMALS

Some of the venomous aquatic animals are a. Vertebrates: Sea snakes, venomous fishes. b. Invertebrates: Shells, mussels, squids, crustaceans, jelly fish. Poisoning by venomous aquatic animals occurs due to: a. Biting: Sea fish. b. Stinging: Spines of various venomous fishes: Stingray, horn sharks, cat fish, scorpion fish, weever fish. c. Surface contact: Jelly fish, sea urchins, blood worm, bristle worm. d. Consumed as food: Shells, mussels, squids, crustaceans (see Chapter 22). Poisoning by Biting/Stinging of Venomous Fish (Table 10.7) Poisoning by Surface Contact Poisoning occurs due to injection of the venom by stinging cells of the invertebrates when they come into contact with the skin of person.

Fig. 10.27: Black scorpion

1. Jelly fish like Portuguese man of war/sea anaemone: Venom contains 5-HT, urocanylcholine.18 2. Molluses or mussels (conch shells, squid, octopus): Venom apparatus cause punctures on the skin and inject venom. 3. Sea urchins: Venomous spines covering their body surface. 4. Bristle worm 5. Blood worm: Bites and inject toxic substances. Clinical Manifestation: In Poisoning by Surface Contact

Local: Pain, swelling, redness. Systemic: Nausea, vomiting, muscular cramps, paralysis, convulsion, collapse, coma, respiratory distress and death. Treatment of Poisoning by Aquatic Animals 1. Washing the area of bite with plain warm water, MgSO4 solution, alcohol or alkaline solution or 1% povidone iodine solution.

It has 2 dorsal spines at Venom is secreted from glandular Sting: Immediate, intense, stabbing anterior margins of two dorsal cell pain with swelling, redness fins. The spines are grooved

Have 3 stings, one dorsal in front of anterior dorsal fin and 2 pectoral stings one in each side in front of pectoral fins

3. Cat fish:

Stinging: Extreme pain with tingling and numbness. Area is firstly ischemic and then becomes red and swollen

6. Weever fish:

The venom is neurotoxic and cardiotoxic

Stinging: Intense pain with swelling

5. Zebra fish and Have 13 dorsal spines, 3 anal – stone fish: spines and 2 pelvic spines with associated venom glands

Have 5–7 dorsal spines and 2 opercular spines with associated venom glands

Stinging: Intense pain + swelling, warm, bluish area surrounding red zone

Sting: Intense pain may lead to shock and death. Secondary infection occurs and takes time to heal

4. Scorpion fish: Have 12 dorsal spines, 3 anal Venom is neurotoxic, spines and 2 pelvic spines haemotoxic and cardiotoxic with associated venom glands

Venomous glands are axillary glands for pectoral stings and glandular structure at base of dorsal sting. The venom is neurotoxic and haemotoxic

Bite: Intense, sharp, shooting, spasmodic or throbbing pain. There is swelling and necrosis of marginal area

2. Horn-sharks:

Venom is secreted from ventrolateral glandular tissue. It causes vasoconstriction and inhibits contraction and dilatation of heart

Sting is present in the dorsal aspect of tail.

Local manifestation

1. Stingray:

Venom gland/venom

Sting/spines

Venomous fishes

Table 10.7: Venomous fishes18

Nausea, vomiting, convulsion, headache, chill, fever, palpitation, bradycardia, cardiac failure, respiratory distress, ankylosis

Nausea, vomiting, convulsion, delirium, fever, pain in joints, respiratory distress and cardiac failure

Nausea, vomiting, convulsion, delirium, fever, pain in joints, respiratory distress and cardiac failure

Respiratory distress

Death due to shock

Nausea, vomiting, diarrhea, faintness, vertigo, drowsiness, sweating, fall of BP, arrhythmia and muscular paralysis (flaccid/spastic)

Systemic manifestation

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2. Analgesic like opiates to relieve pain 3. Application of antihistaminic cream locally. 4. Antibiotics to prevent secondary infection due to bite. 5. Symptomatic 6. Tetanus immunization. ML Aspect of Poisoning by Aquatic Animals 1. Accidental. 2. Poisoning occurs in divers. IMPORTANT QUESTIONS

1. Classify snakes with examples. Describe clinical manifestation and treatment of ophitoxemia (snakebite poisoning). Write difference between cobra and viper. 2. Write difference between venomous and non-venomous snakes. Describe clinical features and management in case of cobra bite. 3. Describe clinical features and management in case of viper bite. Describe postmortem findings and medicolegal aspect of ophitoxemia. 4. Write difference in clinical manifestation of Colubrine bite and Viperine bite. Describe laboratory diagnosis of ophitoxemia. Add a note of anti-snake venom. SPECIFIC LEARNING OBJECTIVES After reading this chapter, the reader should be able to: • Define envenomation and venom • Classify snakes on the basis of their families and on the basis of venom • Enlist common poisonous (venomous) and non-poisonous (non-venomous) snakes in India • Differentiate between poisonous and nonpoisonous snakes • Identify common poisonous snakes in India from its peculiar features and to differentiate the belly and tail scales of Cobra, Krait and Viper • Distinguish between king cobra and common cobra

• Distinguish between cobras and vipers • Explain the features of snake venom • Explain clinical features of snakebite poisoning—envenomation (cobra, viper, krait and sea snakes) • Compare clinical manifestations of colubrine bite and viperine bite • Diagnose ophitoxemia (snake bite poisoning) • Understand the management in snakebite poisoning • Summarize antisnake venom with respect to indications, types and doses in colubrine bite and viperine bite • Explain clinical features and treatment in scorpion bite, bee bite and wasp bite References 1. Weinstein Scott, Dart RC, Staples A, White J. Envenomations: An overview of clinical Toxinology for the primary care physician. American Family Physician. 2009; 80 (8): 793–802. 2. David AW, Guidelines for the clinical management of snake bites in the South East Asia region. New Delhi: World Health Organization, Regional office for South East Asia, 2005:1–67. 3. Roland Bauchot, ed. (1994). Snakes: A Natural History. New York: Sterling Publishing Co., Inc. p. 220. ISBN 1-4027-3181–7. 4. World Health Organization. http://apps.who. int/bloodproducts/snakeantivenoms/ database/default.htm 5. Sarangi A, Jena I, Sahoo H, Das JP. A profile of snake bite poisoning with special reference to haematological, renal, neurological and electrocardiographic abnormalities. J Assoc Physicians India. 1977 Aug; 25(8):555–60. 6. Longo DL, Fauci AS, Kasper DL, Hauser SL, Jameson JL, Loscalzo J. (edi). Disorder caused by venomous snake bites and marine animal exposures. In: Harrison’s Principles of Internal Medicine. McGraw Hill Companies: New York. 18th edn. (vol 2), 2012:3566–83. 7. Bardale R. Principles of Forensic Medicine and Toxicology. 1st edn, Jaypee Brothers Medical Publishers (P) Ltd: New Delhi. 2011:477–87. 8. Ambade VN, Borkar JL, Meshram SK. Homicide by direct snake bite: a case of contract killing. Med Sci Law. 2012; 52:40–3.

Animal Irritants 9. Singhal SK. Singhal’s Toxicology at a glance. 9th edn, National book depot:Mumbai.2016:62–6. 10. Reid HA, Theakston RBG. The management of snakebite. Bull of WHO 1983; 61(6):885–95. 11. Grenvik AKE, Ayers SM, Holbrook PR, Shoemaker WC (editors). Injuries by venomous and poisonous animals. In: Textbook of Critical Care 4th ed 2000: 224–33 [Ref list] 12. Mehta SR, Sashindran VK. Clinical Features And Management Of Snake Bite. Med J Armed Forces India. 2002 Jul; 58(3):247–9. doi: [10.1016/S03771237(02)80140-X] 13. Dikshit PC. Textbook of Forensic Medicine and Toxicology. 2nd edn, PEEPEE Publisher and Distributors (P) Ltd. New Delhi. 2014:509–22. 14. Weatherall DJ, Ledingham JGG, Warrell DA, editors. 3rd ed. I. Oxford Medical Publications; 1996. Injuries, envenoming, poisoning, and allergic reactions caused by animals; pp. 1126–39. (Oxford Textbook of Medicine). [Ref list]

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15. Malani Ajit, Keoliya Ajay. Snake Bite-Bacterial Flora and Role of Antibiotics. Medico-Legal Update. 2016; 16(2):6–11. Article DOI: 10.5958/ 0974-1283.2016.00049.9 16. Tripathi KD. Cholinergic system and drugs. In: Essential of Medical Pharmacology. Jaypee Brothers Medical Publishers (P) Ltd: New Delhi, 7th edn, 2014:99–112 (110). 17. Tripathi KD. Vaccines and Sera. In: Essential of Medical Pharmacology. Jaypee Brothers Medical Publisher (P) Ltd: New Delhi, 7th edn, 2014:919– 27. 18. Nandy A. Principles of Forensic Medicine. New Central Book Agency (P) Ltd: Calcutta, 2nd edn Reprint, 2004:506–16. 19. Aggrawal A. Homicides with snakes: a distinct possibility and its medicolegal ramifications. Anil Aggrawal’s Internet J Forensic Med Toxicol. 2003; 4:1–8.

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Somniferous Poison: Opium and its Alkaloids

11

Somniferous poison/drugs: These are the sleep inducing drugs obtained or derived from the Papaver somniferum plant. It includes opium and their alkaloids. Opium is a dark brown resinous material and has a peculiar smell and bitter taste. It is obtained by giving incision to the unripe fruit (poppy capsule) of Papaver somniferum (poppy plant). It is the milky exude which on exposed to air becomes dark brown or black crude opium commonly called “Afim”.

Plant: Papaver somniferum is a herb growing up to a length of 1 meter. Flowers are large purple white or white in color. Each plant bears 5–10 fruits (poppy capsules) containing numerous small poppy seeds. The plant is a native of Turkey and is cultivated worldwide under Government control. In India, it is cultivated and distributed in Ghaziabad, Uttar Pradesh under Government supervision and also in Rajasthan and Madhya Pradesh. Opium has 20 alkaloids of which morphine is most important. A dried poppy capsule contains little narcotine.1

Fig. 11.1: Poppy plant

Types of opiates and active principle: It has alkaloids classified as:2 1. Natural: It has two groups: a. Phenanthrene: Morphine, codeine and thebaine. b. Benzyl isoquinolene: Papaverine, noscapine/narcotine and narcine. 2. Semisynthetic opiates: Diacetyl morphine (heroin), dehydromorphine, oxymorphone, hydromorphone, hydrocodone, oxycodone, N-allyl-normorphin (nalorphine). 3. Synthetic opiates: Pethidine, fentanyl tramadol, methadone hydroxypethidine. .

Fig. 11.2: Incised unripe poppy capsules 138

Fig. 11.3: Afim-crude

Somniferous Poison: Opium and its Alkaloids

Uses 1. Morphine and codeine have maximum use as analgesic and cough depressant respectively. 2. Poppy seeds (khas-khas) are used in different food preparations. 3. Heroin is used as cough suppressant and is a drug of addiction. 4. Pethidine is used as analgesics. A single dose of pethidine may make an individual addict. 5. Morphine being respiratory depressant, is contraindicated in head injury and is a drug of addition. 6. Apomorphine, prepared from morphine is used as an emetic. Mechanism of Action • It causes CNS depression and narcosis (analgesic + hypnosis). • It depresses all centres (in cortex and medulla—respiratory and cough) except vomiting centre, occulomotor centre and sweating (vagus).1 Fatal dose: Opium—2 gm, morphine—100– 200 mg, codeine—500 mg, heroin—50 mg, pethidine—1 gm, methadon—100 mg. Fatal period: 6–12 hours. Absorption, Fate and Excretion • It is absorbed through mucous membrane of GIT. When smoked, it is absorbed through lungs. • Metabolised in liver. • Excreted through kidneys, bile, milk, saliva and also through stomach and intestine. SIGNS AND SYMPTOMS

Poisoning occurs due to ingestion of opium or its alkaloids or injection of morphine. In Tehran (Iran), 41.54% of the poisoning deaths were due to opioid alone followed by other drugs and organophosphates.3 There are 3 stages of opium poisoning:1,4,5 Stage I: Stage of Excitation and Euphoria

• There is excitement, increased sense of wellbeing, increased mental activity, flushing of

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face, increased pulse hallucinations and convulsion. • But soon there is restlessness, anxiety, dizziness, nausea and dysphoria. Stage II: Stage of Depression or Stupor Headache, giddiness, drowsiness, dizziness, disorientation, ataxia, lack of interest/ concentration, uneasy feeling, contracted pupils, cyanosed face and generalized itching. Stage III: Stage of Narcosis/Coma

• Muscles relaxed, reflexes are lost, pinpoint pupils • There is hypotension, Cheyne-Stokes breathing, sweating, hypothermia (due to reduction in oxygen consumption, low metabolic activity and failure of heart regulating mechanism), cyanosis and froth at mouth and nose (due to pulmonary edema 6 ) with progressive respiratory depression. • Pulse is slow, and skin is moist, cold, clammy, and pale. Face is flushed, conjunctiva suffused. • There is constipation due to constriction of smooth muscles of the sphincter. Emptying of stomach is delayed. • There is oliguria, hyperglycemia, glycosuria and renal failure. • There is uneasiness, sleep, coma and death. DIAGNOSIS OF OPIUM POISONING

The triad5 of following features strongly suggests opium poisoning: • Coma, • Pinpoint pupils, • Depressed respiration, along with • Typical opium smell (raw flesh) • Cyanosis • Froth at mouth and nostrils • Cheyne-Stokes breathing • Slow pulse, bradycardia • Moist cold skin and hypothermia.

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DIFFERENTIAL DIAGNOSIS

• Alcoholic intoxication, barbiturate/ carbolic acid/CO poisoning • Cerebral malaria/encephalitis/meningitis, • Epileptic coma, hysterical coma, cerebrovascular accidents (IC hemorrhage with compression of the brain) • Heat stroke • Uremia, diabetic coma TREATMENT

1. Stomach wash with 1 : 5000 dilution of KMnO4. About 200 ml of the solution is left in the stomach after last wash to neutralize morphine, which is resecreted in the stomach after absorption even if morphine has been injected.2 2. Enema and purgatives: 20 gm MgSO4 3. Antidote: Naloxone (is an opioid antagonist): 0.4–0.8 mg IV every 2–3 minutes till respiration improves2 and dilatation of pupil. Naltrexone—long acting preopioid antagonist can be given three times a week at the dose of 100–150 mg orally.7 Newer antidote is Nalmefene 0.1 mg IV followed by 0.5 mg IV. Methadone is used in chronic poisoning. However, opioid antagonists can precipitate acute

withdrawal symptoms in chronic opioid users.8 4. Safeguarding respiration: • Bronchial suction to make airway free from secretion. • Artificial respiration and O2 inhalation • Endotracheal intubation to ensure free air passage. 5. Stimulants: Methyl amphetamine HCl— 10–20 mg, acts as stimulant to different system. Coramine as cardiorespiratory stimulant. 6. Supportive: • Antibiotic to prevent pulmonary infection. • Correction of fluid and electrolyte imbalance. • Benzodiazepines for convulsion. POSTMORTEM FINDINGS External

• Face congested with deep cyanosis over lips, ear lobules and nailbeds. • Black postmortem lividity. • Froth at mouth and nostrils. • Smell of opium (raw flesh) present. • Features of drug addiction—injection marks with pigmented and scar formation and tattooing.

Fig. 11.4: Poppy seeds and dry poppy capsules

Somniferous Poison: Opium and its Alkaloids

Internal

• Stomach: Contents have characteristic smell with presence of opium ingredients. • Respiratory tract: Froth present.7 • Lungs: Congested, edematous 7 • Brain: Congested, edematous with petechial hemorrhage on cut section. • Blood: Dark and fluid. • Visceral organs congested. MEDICOLEGAL ASPECTS

1. Suicidal: It is a popular suicidal agents leading to painless death. 2. Homicidal: Not used due to its bitter taste, characteristic smell, and delayed death. 3. Accidental: Due to overdose in addicts and in children; and due to therapeutic misadventure.

(a)

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4. Aphrodisiac: Morphine is used to increase sexual desire but it diminishes the performance. 5. Addicts can consume high dose of morphine/opium. There is moral degradation, and lack of judgment which may lead to commit any crime getting the drug out of desperation.1 CHEMICAL TEST

Marquis Test for Morphine Put one drop of mixture (3 ml of conc. H2SO4 + 3 drops of formalin) on a blotting paper soaked with test material. If the test material contains opium or morphine, then there is a play of color from purple to violet and finally blue.

(b) Fig. 11.5: Heroin/brown sugar

Opium/morphine addiction

Withdrawal symptoms in opium addict

Features of addiction (morphine mania) 1. Irritability, fatigability, lack of interest/ concentration, loss of weight and appetite, constipation, furred tongue, impotence/ frigidity 2. Mental and moral degradation, loss of self respect and morality and a desire to procure drug by any means 3. For parentral use (skin popping in SC use and main lining in IV use): There will be pigmentation and scar formation at the site of injection often masked by artificial tattooing1 4. Toxic dementia may develop

Features of withdrawal 1. Restlessness, anxiety, nervousness, insomnia, drug seeking behavior 2. Running nose, yawning, sweating, scratching, shivering, hot and cold flushes, goose skin appearance, dilated pupil. 3. Severe twitching of muscle/muscle spasm, painful cramps in legs, tremor with vomiting, diarrhea, abdominal pain, loss of weight and appetite. 4. Dangers: There may be debility, injury, intercurrent infection

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Treatment of opium addiction1 1. Gradual withdrawal of drug 2. Substitution therapy with methadone 30–40 mg/day and then gradually tapered off 3. -Adrenergic blocker like propranolol (80 mg) is quite effective in anxiety and craving 4. Maintenance of food, nutrition and vitamins 5. Nursing care 6. Physical restrain 7. Psychiatric counseling

Treatment of withdrawal symptoms1 1. Chlorpromazine 50–100 mg or pentobarbitone 2. Low dose of morphine or methadone 3. Physical restrains to protect from accident and injury 4. Maintenance of food, nutrition and vitamins 5. Nursing care 6. Antibiotic in some cases 7. Naloxone HCl: 0.4–0.8 mg IM/IV (0.01 mg/kg in children)4

Other opiates Codeine (methyl morphine): (Natural) It is popularly used as cough depressant. It is also used as an analgesic. It is less toxic than morphine and is less miotic, less constipating and more nauseating.1 It has been used to control diarrhea2 In toxic doses, it excites medulla and spinal cord and causes convulsion and delirium

Pethidine and methadone (synthetic opiates) Pethidine is good analgesic, narcotic and sedative and causes mydriasis and dryness of skin. It liberates histamine from mast cells.1–4 It has direct inhibitive action on heart muscles4

Brown sugar: It is crude heroin (semisynthetic) Heroin (diacetyl morphine) It is semisynthetic opiate derived from morphine, which is 2–3 times more toxic than morphine.1 It is a white to dark brown colored powder. It is more lipid soluble, therefore, enters the brain more rapidly. So, it causes more euphoria and addiction than other narcotic drugs2 It is ‘downer’ or depressant drug that affects the brain’s pleasure system and interferes with the brain ability to perceive pain.

Nalorphine (N-allyl-normorphine): Semisynthetic opiate It causes analgesic, respiratory depression, dysphoria, and hallucination.1 It was popularly used as an antidote to morphine but because of its dysphoric and psychotomimetic effects, it is not used nowadays.2

IMPORTANT QUESTIONS

1. How opium is obtained? Write classification of opiates. Describe action, clinical manifestation, treatment, postmortem findings and medicolegal aspect of morphine poisoning. 2. What is afim? Write mechanism of action and management of morphine poisoning. Add a note on opium addiction and withdrawal symptoms. SPECIFIC LEARNING OBJECTIVES

After reading this chapter, the reader should be able to: • Define afim/opium • Name the somniferous poisons

• Recognize various types of opiates with examples • Enumerate different uses of opiates • Understand the mechanism of action of opiates • Explain clinical manifestations of poisoning due to opium/ morphine • Recognize diagnostic features of opium poisoning • Enumerate differential diagnosis of morphine poisoning • Explain the management in opium/ morphine poisoning • Explain postmortem findings and medicolegal aspect of morphine poisoning • Illustrate chemical test for morphine

Somniferous Poison: Opium and its Alkaloids

References 1. Nandy A. Principles of Forensic Medicine. New Central Book Agency (P) Ltd: Calcutta, 2nd edn Reprint, 2004: 517–43. 2. Tripathi KD. Opioid Analgesic and antagonists. In: Essential of Medical Pharmacology. Jaypee Brothers Medical Publisher (P) Ltd: New Delhi, 7th edn, 2014: 469–85. 3. Shadnia S, Esmaily H, Sasanian G, Pajoumand A, Hassanian-Moghaddam H, Abdollahi M. Pattern of acute poisoning in Tehran-Iran in 2003. Human & Experimental Toxicol. 2007; 26, 753–6. 4. Dikshit PC. Textbook of Forensic Medicine and Toxicology. 2nd edn, PEEPEE Publisher and Distributors (P) Ltd. New Delhi. 2014: 547–52.

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5. Bardale R. Principles of Forensic Medicine and Toxicology. 1st edn, Jaypee Brothers Medical Publishers (P) Ltd: New Delhi. 2011: 508–10. 6. Silber R, Clerkin EP. Pulmonary edema in acute heroin poisoning: Report of four cases. The American Journal of Medicine. 1959; 27(1):187–92. 7. Longo DL, Fauci AS, Kasper DL, Hauser SL, Jameson JL, Loscalzo J. (edi). Opioid drug abuse and dependence. In: Harrison’s Principles of Internal Medicine. McGraw-Hill Companies: New York. 18th edn. (vol 2), 2012: 3552–6. 8. Allen SC. Problems with naloxone (letter). BMJ1975;3:434. Google Scholar. 9. Jaiswal AK, Millo T. Screening/spot/color test for different poisons. In: Handbook of Forensic Analytical Toxicology. 1st edn, Jaypee Brothers Medical Publishers (P) Ltd: New Delhi. 2014: 81–174.

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12 Inebriant Poison: Alcohols Inebriant means to cause drunkenness or to intoxicate. It includes alcohols and their derivatives, anesthetic drugs, and fuels like kerosene and petrol. These are the poisons, which are characterized by two sets of manifestations: 1. Excitement 2. Narcosis—it is the combination of hypnosis + analgesia. Definition of alcohol: It is an organic hydroxy compound obtained by replacing one or more hydrogen atoms from aliphatic hydrocarbons by hydroxyl group (–OH). Thus, alcohols are hydroxyl derivatives of aliphatic hydrocarbons. Absolute Alcohol is 99% concentrated. Alcohol is obtained by enzymatic fermentation of: Carbohydrates (sugars and starch); Raw materials (cereals, corn, barley, etc.); Jaggery; Molasses; Potatoes; Fruits (grapes, oranges, cashew nut, etc.); and flower (mohua). The fermentation is followed by process of distillation and non-distillation method. If it is obtained by distillation method, then it is called spirit.

Spirit: Means any liquor containing alcohol and obtained by distillation after fermentation (whether denatured or not)

Liquor: Term used for any liquid containing alcohols obtained by any method (distillation includes spirits like brandy, gin, rum, vodka, whiskey, etc. or not distilled includes wine, beer, toddy, etc.)

Rectified spirit: It is the spirit subjected to rectification (process whereby liquor is purified or refined) for making it potable (Fig. 12.1)

Denatured spirit: It is the spirit subjected to a process for the purpose of rendering unfit for human consumption, e.g. French polish, varnish (Fig. 12.1)

Methylated spirit (industrial): Rectified spirit with Surgical spirit: 95% ethanol + 5% methanol + oil of 5–10% wood naphtha (i.e. impure methyl alcohol) wintergreen (sweetish flavor for easy detection and so as to render it unfit for drinking. It can be applied pleasant use) on skin as antiseptic, cleaning and astringent purpose1 Beverages are drinks used for their flavor or stimulating effect, e.g. tea, coffee, aerated water, wines, etc. These may be alcoholic or non-alcoholic

Toddy is liquor not a spirit. It means fermented or unfermented juice extracted from palm tree, e.g. coconut, barb, date, etc. Neera is unfermented juice extracted from any palm tree

Arrack is an Eastern name for any country liquor • Distilled from rice/sugar or jaggery, cashew nut, coco palm, and mohua flowers. 144

• Fortified with powerful knock out agents like potassium bromide, chloral hydrate, datura and bhang.

Inebriant Poison: Alcohols

145

Fig. 12.1: Rectified and denatured spirit

Different names for liquor: Andhra Pradesh—Gudamba; Maharashtra—Khopri; Gujarat—Lattha; Goa—Feni; Mexico—Tequila; Japan—Sake.

Fig. 12.3: Wines—Champagne, port

vodka, whisky, etc. It is standardized to 42.8% v/v or 37% w/w (Fig. 12.4).

Alcoholic Beverages1 a. Malted liquor: Obtained by fermentation of germinating cereals; are un-distilled with alcohol content of 3–6%, e.g. Beers, Stout (Fig. 12.2).

Fig. 12.4: Spirits: Whisky, vodka, gin, rum Table 12.1: Alcohol percentage in different beverages

Fig. 12.2: Malted liquor—beers

b. Wines: Obtained by fermentation of natural sugars present in grapes and other fruits. These are also un-distilled containing 9–22% alcohol, e.g. claret, cider, port, sherry, champagne (Fig. 12.3). c. Spirits: These are distilled after fermentation, e.g. Brandy, gin, rum,

Beverages

Origin

Alcohol % by volume

Proof %

Rum Whisky Brandy Gin

West Indies Scotland – Holland

75 75 75 65–75

Beer Country liquor

Brazil

42.8 42.8 42.8 42.8/40.0/ 37.2 2–10.0 11.4–45.7

3.5–17.5 20–80

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Vodka is the purest form of beverages and does not contain any congeners. It is virtually odorless. One peg: Large peg = 60 ml and small peg = 30 ml. Patiala peg = 90 ml Types of drink Soft

04–08% alc Beer

Moderate 10–20% alc

Wines, champagne

Hard

Whisky, brandy, gin, rum

40–55% alc

Proof spirit (57.10%) defines such strength of alcohol which when poured onto gunpowder allowed it to burn, since the remaining 42.90% of water did not prevent it. It indicates a mixture containing 57.10% by volume (or 49.28% by weight) of absolute alcohol (Fig. 12.5).

Uses 1. Beverages/drink: It is used as a drink for pleasure and to reduce tension. 2. Solvent: For after-shaves, colognes, mouthwash, perfumes (15–80%). 3. Preservatives: Rectified spirit is used as preservatives of viscera for chemical analysis. 4. In industries and laboratories. 5. Medicinal uses: a. Surgical spirit is used as an antiseptic. b. Several multivitamins and cough syrups contain varying amount of alcohols— 2–20%. c. Antidote for methanol and ethylene glycol poisoning. d. Ethanol sponging is an effective remedy for hyperthermia.1 e. It is also used in trigeminal neuralgia.1 6. Decreases the risk of occlusive coronary disease and embolic strokes:2 Relatively low doses of alcohol (1 or 2 drinks/day) have potential beneficial effects of increasing HDL cholesterol and decreasing aggregation of platelets. It also decreases the risk of vascular dementia and possibly Alzheimer’s disease. Action CNS—excitation followed by depression. It removes the restraints on primitive behavior.

Fig. 12.5: Showing proof spirit—75° proof

Proof strength of a liquid is obtained by dividing the alcohol percent in volume by 0.571, e.g. wine—10% alcohol. Therefore, proof spirit = 10/0.571. Similarly % of alcohol in liquid is obtained by multiplying the proof strength by 0.571, e.g. brandy 75o proof = 75 × 0.571= 42.8% by volume. ETHYL ALCOHOL: C2H5OH

Properties: Colorless, sweetish/fruity (apple like) or acetone smell, sweet piercing taste, soluble in water.

Fatal dose: For non-addicts: 150 ml at a time rapidly. Fatal period: 12–24 hrs. Absorption, Distribution, and Excretion Absorbs rapidly from intestine (proximal part), but also from the mucosa of mouth, esophagus, stomach and large bowel.2 The rate is more than glucose. Alcohol is distributed in intracellular and extracellular fluid of the tissue. ‘Walked off’— exercise sharply fall of alcohol supply to the brain. 2–10% of ethanol is excreted directly through lungs (breath), urine or sweat. But

Inebriant Poison: Alcohols

147

90% is excreted/metabolised to acetaldehyde primarily in liver.2 Absorption of Alcohol Depends on

1. Amount of food in stomach: Empty— absorbs rapidly. 2. Quality of food: Fat and protein—delays absorption. 3. Concentration of alcohol: a. Higher concentration is absorbed rapidly due to irritation and inflammation of gastric mucosa. b. But in chronic user, it is not rapidly absorbed as higher concentration destroys the mucosa. c. The absorption is maximum at 20% v/v dilution of ethanol.2 4. Presence of CO2: Increases absorption by increasing the absorption surface and induce rapid gastric emptying.2 5. Condition of stomach wall: Gastrectomy, chronic gastritis—increases the absorption. 6. Quantity and rate of drinking. 7. Weight of person. 8. Development of tolerance. Metabolism Ethyl alcohol  acetaldehyde  acetic acid  CO2+H2O 80% of the ethanol is oxidized by alcohol dehyrogenase and then aldehyde dehydrogenase i n t h e c e l l cy t o s o l a n d mi t o c h o n d r i a ( F i g . 12.6). But 20% metabolized in the microsomes of the smooth endoplasmic reticulum called microsomal ethanol oxidizing system (MEOS).2 Oxidation yields 7 cal of energy/gm and causes reduction of intake of other food by alcoholic (vitamin and nutrients), leading to degenerative changes in liver.3 Blood Alcohol Concentration (BAC) Blood levels of ethanol are expressed as milligrams or grams of ethanol/decilitre (e.g. 100 mg/dL = 0.10 g/dL) or milligram/ml of blood (e.g. 100 mg/100 ml = 0.1% = 0.1 g/dL) with values of ~0.02g/dL resulting from ingestion of one typical drink.2

Fig. 12.6: Alcohol metabolism

Blood alcohol level reduces by about 10 mg% per hours and about 7 ml is washed out per hour in this way. BAC reaches a maximum (peak) in about 1 to 1½ hours after ingestion. However, it is present in the blood within 30 min and urine within 60 min. Level of alcohol in mg/100 ml of blood (BAC) 50 (0.05%)

Minimum consumed volume of 75° proof spirit in ml 69.5 ml

100 (0.1%)

139.0

200 (0.2%)

278.0

300 (0.3%)

417.0

400 (0.4%)

556.0

500 (0.5%)

695.0

Acute poisoning: Result from consumption of any preparation containing alcohol either in small doses at short interval or one big dose. Clinical Features and Stages I. Stage of excitement: 0.05% to 0.1% blood alcohol (>0.1% not fit to drive a vehicle) • Inhibits the higher centers, which controls judgment and behaviour leading to unrestrained and unabstained character of a person. • There is loss of restraints of code of conduct (habit, duty, behavior).

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• • • •

The person becomes excited and talkative. Skin—flushed, warm (increased temperature). Conjunctiva—reddened or congested. Pupils—dilated, sluggish reacting to light/ accommodation. • Smell of alcohol present in breath. • Pulse increased, HR/BP increased. II. Stage of in-coordination (0.1 to 0.3%) There is in-coordination of: Thought—recent memory impaired Speech—slurred, incoherent Action (incoordination of muscle)—staggering gait, and skill movement impaired and reaction time increased. • Impaired judgement • Eyes—suffused, • Vision—blurred, double, • Pupil—dilated, sluggishly reacting to light, • Mouth—dry, and • Tongue—furred. III. Stage of narcosis (0.3 to 0.5%) • Deep sleep responds to strong stimuli • Pulse—rapid, temperature—subnormal, • Pupil—constricted,

• Macewen’s sign present (pinching of skin of neck/face leads to dilation of pupil). • A fine lateral nystagmus—oscillatory movement of eyeball (alcoholic gaze nystagmus—AGN). Alcohol causes nystagmus by two mechanisms. 1. Firstly by acting on vestibular system, it causes positional alcoholic nystagmus (PAN), when the person is lying supine with head turned either left or right. 2. Secondly by inhibiting smooth pursuit system due to alcohol effect on ocular movement via neural mechanism results in horizontal gaze nystagmus (HGN). IV. Stage of medullary paralysis (>0.5%): • Slow, stertorous respiration, • Cold calmly cyanotic skin, • Dilated pupil, abolished reflexes, very weak pulse, • Dilated pupil, • Abolished reflexes, very weak pulse. Chronic poisoning: Result from continued use of alcohol and is characterized by physical, moral and mental deterioration. Physical: Lack of personal hygiene, loss of appetite, gastroenteritis, wasting, peripheral

Treatment—acute alcoholic

Treatment—chronic alcoholic

1. 25% dextrose drip

1. Gradual withdrawal of alcohol

2. Inj B1 (thiamine) 100 mg IM stat followed by 100 mg thiamine in 500 ml glucose IV infusion1 daily till the patient becomes conscious. Then, switch to oral B-complex

2. Antabuse: Disulfiram—It is alcohol dehydrogenase inhibitor; and produces vomiting and autonomic nervous system instability due to accumulation of acetaldehyde in the blood.2 Dose:1 500 mg × 7 days followed by 250 mg daily. It should be given only when the patient has not consumed alcohol within 12 hours and who sincerely desire to leave the habit.

3. Proton pump inhibitor: Inj pantoprazole/ rabeprazole/ranitidine

3. Citrated calcium carbimide (CCC):3 Temposil—50 mg—OD (similar to antabuse)

4. Sucralfate—if GIT bleeding

4. Chlorpromazine— 50 mg

5. IV fluids maintenance

5. Diet

6. Respiration is safeguarded by artificial respiration and O2 inhalation, if needed

6. Supportive

7. Stomach wash, if required

Inebriant Poison: Alcohols

neuropathy, fatty changes in liver and heart, impotence and sterility. Moral: Wide sociological abnormalities. Mental: Loss of memory, impaired judgement. Thus, there is GIT disturbance, liver damage with jaundice, ascitis, peripheral neuritis, tremor, insomnia, intermittent infection. 3 Approximately 35% of drinkers experienced temporary anterograde amnesia and disturbed sleep.2 Complication resulting from chronic alcoholism (alcohol withdrawal syndrome) 1. Delirium tremens: It is a psychotic condition in chronic alcoholic and its withdrawal. It is characterized by tremor, convulsions, insomnia, amnesia, confusion, disorientation, and failure to recognize known things, hallucination and agitated behavior Causes i Sudden increase in quantity ii. Sudden withdrawal of alcohol iii. Injury/infection iv. Shock from injury v. Exposure to cold Treatment3 i. Largactil—100 mg orally ii. Meprobamate—2.4 gm daily iii. Sedation—phenobarbitone, paraldehyde or chlorpromazine injection is given iv. 5% dextrose IV drip, vitamins v. Symptomatic 2. Korsakoff’s psychosis: It is a psychological and neurogenic deranged condition occurring in some alcoholics.3 It is characterized by hallucinogens, disorientation, multiple neuritis and muscular degeneration, i.e. weakness, wasting and unsteady gait, retrograde amnesia—loss of recent memory. 3. Acute hallucinosis: Auditory hallucinogens, delusion of persecution. 4. Alcoholic confusional insanity: It is one of the withdrawal problems in chronic alcoholic with disorientation of time and place, hallucinations, delusions and mania/attack.

PM Findings • Clothes are dirty, torn, soiled with vomitus and earth particle. • There may be minor and major external injuries.

149

• Visceral organs are congested. • Stomach contents—smell of alcohol with mucosa congested, hemorrhagic at places. • Lungs and brain are congested and edematous. • Liver may be cirrhotic, fatty. • Other signs of hazards of alcohol may be present. Material Preserved 1. Routine viscera—in saturated solution of common salt. (Rectified spirit—not to be used.) 2. Blood—in sodium fluoride/oxalate. 3. Urine—without any preservatives. Medicolegal Aspects 1. Alcohol causes death mostly due to its associated hazards. 2. Accidental death—due to inhalation of vomitus or due to adulterated drinks or due to consumption of synergistic drug along with alcohol. 3. Suicide—alcohol is commonly used with other poison to commit suicide. Poisons were also taken under the influence of alcohol. 4. Homicide—for this the poison is mixed with alcohol to mask taste and smell. The person was killed by inflicting fatal injury or by pushing from height or by drowning after intoxicate by giving alcohol. 5. Aphrodisiac agent—it is used to increase sexual desire but it decreases the performance. 6. It is used to accomplish a criminal act or to give strength before committing crime. Hazards Associated with Alcohols

1. Vehicular accidents. 2. Fall from height. 3. Electrocution/drowning/burns 4. Choking-café coronary 5. Cooking gas poisoning 6. Death

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Forensic Toxicology: A Comparative Approach

7. Saturday night paralysis—by compression of circumflex nerve. In intoxicated condition, the person rests his armpit on the back of his chair causing sustained pressure on circumflex nerve leading to temporary paralysis of his arm. CHEMICAL TEST: DICHROMATE TEST

Filter paper soaked with potassium dichromate is placed at the mouth of test tube containing test material (urine). Heat the test tube for 1 min. If alcohol is present, color of filter paper changes from orange to green. DETERMINATION OF BLOOD/ URINE ALCOHOL

1. Kozelka-Hine/Cavett method—aeration/ distillation method: Potassium dichromate or H 2 SO 4 Alcohol acetic acid Oxidized

Each ml of 0.05 N dichromate solution that is reduced in the process is equivalent to 0.575 mg of alcohol. 2. Gas chromatography 3. Alcohol dehydrogenase method 4. Breathalyzer—it is a device for estimating blood alcohol concentration (BAC) from a breath sample (Fig. 12.10). The driver/

Fig. 12.7: Submucosal hemorrhage of stomach in acute alcoholic intoxication

rider is asked to blow through the plastic tube, the level of alcohol is displayed on the screen. It is legally admissible as per the section of MV Act, 1988. The false positives are4: Mouthwash containing alcohol used within 20–30 min, hyperventilation, physical exercise, emesis, regurgitation of stomach content. WIDMARK FORMULA

It is used to estimate alcohol absorbed in the body by • a = CPR , therefore C = a/PR • R is the constant, for male = 0.68, for female = 0.54, • C is the blood alcohol concentration (gm/kg); ‘a’ is the total amount of alcohol in gm absorbed in the body. P = Weight of person • For urine, a = 3/4 qpr, where q is the concentration of alcohol in urine (gm/L) • Example: 70 kg male has consumed 120 ml of 25° proof liquor. What will be the blood alcohol level? • a = CPR, but proof spirit and density of alcohol (ml/kg) consumed should be considered for calculation. Therefore, C = a × proof spirit × density of alcohol/PR = 120 × 0.428 × 0.8/70 × 0.68 = 86 mg%

Fig. 12.8: Cirrhosis of liver in chronic alcoholic

Inebriant Poison: Alcohols

Fig. 12.9: Ethanol and denatured spirit

151

Fig. 12.10: Breathalyzer

METHYL ALCOHOL: CH3OH (METHANOL)

ISOPROPYL ALCOHOL: C3H7OH

It is a volatile, colorless, flammable liquid with distinct odor similar to ethanol, but highly toxic and unfit for human consumption (Wood naphtha/spirit)

It is a colorless flammable liquid with a strong odor, used in disinfecting pads/hand sanitizers It is 3 times more toxic than methyl alcohol, which is more toxic than ethyl alcohol

Uses 1. Used as industrial solvents 2. With ethanol, used as antiseptic spirit 3. Methylated spirit = Mixture of ethanol + methanol 4. Embalming fluid, leather dyes, paint remover, varnish

Uses 1. Used as industrial solvents 2. Used as gasoline additive 3. Alternative to formaldehyde as tissue preservatives 4. Antiseptic spirit/hand sanitizer.

Fatal dose: 60–120 ml

Fatal dose: >100 mg% in blood

Fatal period: 24–36 hours

Fatal period: A few hours

Action: CNS depression.

Action: Cerebral depressant and renal damage as it oxidizes to acetone.3

Absorption, distribution, excretion Same as ethanol. However, methanol is metabolized to formaldehyde and formic acid by alcohol dehydrogenase and aldehyde dehydrogenase respectively, but the rate is 1/7th that of ethanol.1 Methyl alcohol  formaldehyde  formic acid

Absorption, metabolism, excretion Absorption through mucosa of GIT/RT. It is metabolised (oxidized) to acetone by alcohol dehydrogenase in liver.5 Excreted through urine as such or acetone, and small amount through breath.

Clinical features • Nausea, vomiting, abdominal pain, epigastric pain, dehydration, smell present. • Tachypnea, dyspnea, bradycardia, low BP, collapse • Headache, dizziness, vertigo, muscular pain/ weakness, cramp, restlessness, disorientation, convulsion, coma. • Acidosis due to formic acid which leads to retinal changes leading to blurring of vision and blindness.1 • Death due to respiratory failure.

Clinical features5 • Nausea, vomiting, abdominal pain, dehydration, smell present • Low BP, hypothermia • Headache, dizziness • Diminish reflexes • Constriction of pupils • Renal damage • Shock, respiratory depression and coma

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Treatment 1. Patient must be hospitalized and kept in quiet dark room. 2. Eyes—covered and protected from light 3. Stomach wash with NaHCO31 4. Combat acidosis by IV NaHCO3 infusion (2 gm in 250 ml water every 2 hrs) prevents retinal damage and other symptoms (dehydration).1,4, 6 Potassium chloride infusion for hypokalemia due to alkali therapy.1 5. Hemodialysis: It clears methanol/ formic acid6 6. Antidote: Oral ethyl alcohol7 and Fomepizole 7. Folate therapy:1 Calcium Leucovorin 50 mg injected 6 hourly to reduce formic acid level.

Fig. 12.11: Mohua plant and seeds

Treatment 1. Stomach wash 2. Symptomatic 3. Protection of the kidneys: • Hemodialysis • Dialysis if renal failure 4. Oxygen therapy to excrete acetone from lungs 5. Fluid replacement if dehydration Clinical diagnosis of methyl alcohol poisoning is made in the presence of high index of suspicion of toxic alcohol ingestion, early visual symptoms, unexplained anion gap metabolic acidosis and significant osmolar gap.7

Fig. 12.12: Mohua flower

Fig. 12.13: Large and small pegs—measurement

Inebriant Poison: Alcohols

153

Specific antidote of methanol poisoning1 1. Ethanol 100 mg/dl in blood saturates alcohol dehydrogenase and retards methanol metabolism and thereby reduces the rate of generation of toxic metabolite. No IV formulation of ethanol is available. Ethanol 10% in water is given through nasogastric tube in a loading dose of 0.7 ml/kg followed by 0.15 ml/kg/hr 2. Fomepizol is a specific alcohol dehydrogenase inhibitor, is given in 15 mg/kg IV followed by 10 mg/kg 12 hrly till serum methanol falls below 20 mg/dl Methyl alcohol

Isopropyl alcohol

PM findings • S/o asphyxia with cyanosis and marked PM staining. • Frothing from mouth with presence of smell. • Stomach/intestine—mucosa congested, alcoholic smell present • Lungs/brain—congested and edematous • Liver—fatty changes • Kidney—tubular degeneration

PM findings • Nothing specific • Visceral organs—congested • Liver/kidneys—congested, edematous • Renal degeneration

ML aspects 1. Accidental: Most of cases are accidental due to adulteration of alcoholic drink with methylated spirit 2. Suicidal and homicidal uses may occur but are not common

ML aspects 1. Accidental—mostly by way of external medicinal use 2. Suicidal—due to easy availability as it is the main ingredient in many cleaning products

Fig. 12.14: Methanol and isopropyl alcohol

Fig. 12.15: Non-alcoholic beverages

Fig. 12.16: Different types of alcoholic beverages

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EXAMINATION OF ALCOHOLIC PERSON

Medical man is often required to examine a person and certify whether the person is under the influence of alcohol or not. So it is examined as per the following proforma: Examination of Alcoholic To The Investigating Officer PS ......................................................................... Ref: Your letter No. ................., dated ............... 1. Name: .............................. Age: ..... Sex: ...... Address: ....................................................... ........................................................................ 2. Identification marks (two) 3. Consent Under Section 53(1) of CrPC: Examination of accused can be carried out by a medical practitioner at the request of police even without his consent and by use of force, if necessary. Brought by PC: ............. No.: ........ PS ......... Date and time of examination: ................... Place of examination: .................................. Examination in presence of: ....................... 4. History of consumption of alcohol/ medication: • Type, duration • Consumption of any mouthwashes • History of diabetes • Past history of: Head injury 5. General behavior: Whether polite, excited, hilarious, talkative, carefree, sleepy, cooperative, indifferent, antagonistic, combating, insulting, etc. (Polite = Polished; Excited = Agitated, roused emotionally; Hilarious = Very funny; Talkative = Repeated talk; Indifferent = Not very good, uninteresting; Antagonistic = One who straggles with other; Combating = Opposing) 6. Memory: Recent event • Whether having orientation of time/ place/person.

• Ask a few personal questions and then ask the same at the end of examination. • Ask about some article/object in the examination room like number of tube light/tables, etc. and then ask the same in the last. 7. Mental alertness: Ask simple sums of addition or subtraction and see how much time person will take. How quickly the person responds to you and your question during examination. 8. Temp 9. Pulse 10. Resp 11. BP 12. Skin: Dry, moist, flushed, pale 13. Smell of alcohol in breath 14. Eye: Normal, watery, congested, suffused. Pupils: Normal, dilated, constricted. Reaction to light: Normal, poor. 15. Gait Balance: Sure, fair, swaying, wobbling, sagging knee, falling other. Walk: Sure, fair, swaying, uncertain, staggering to reel. Turning: Sure, fair, swaying, uncertain, staggering to reel. (Sure = Safe; Fair = Clear; Swaying = Incline from side to side; Wobbling = To move unsteadily from side to side; Sagging knee = To bend; Uncertain = Lacking confidence) 16. Speech: Whether fair, slurred, stuttering, confused, incoherent, other. (Slurred = Blurred; Stuttering = To speak, say or pronounce with spasmodic repetition of words, especially initial; Confused = Disordered; Incoherent = Loose) 17. Muscular coordination Finger nose test: Sure, uncertain. Picking up coins: Sure, slow, uncertain, unable. Unbuttoning and buttoning of shirt. 18. Handwriting and copying of sentence: Missing of letters; not in straight line

Inebriant Poison: Alcohols

19. Reflexes: Knee and ankle: Delayed and sluggish. 20. Systemic examination RS CVS P/A 21. Investigation Blood: Spirit must not be used Preservatives: 10 mg sodium fluoride + 30 mg Potassium oxalate per 10 ml of blood Urine: 100 ml Preservatives: 30 mg phenyl mercuric nitrate for 10 ml urine or 5 ml conc. HCl for 200–500 ml urine. Note: The samples are preserved, sealed and handed over to police on duty at the earliest for chemical analysis.

Opinion 1. The above person has not consumed alcohol. 2. The above person has consumed alcohol but is not under its influence. 3. The above person has consumed alcohol and is under its influence. Place ............................. Signature ............. Date ............................................................... Name of doctor ............................................ Time .............................................................. Designation .................................................. Seal ................................................................ But, the opinion whether the person is under or not under the influence of alcohol is purely based on the clinical examination. The signs and symptoms of alcoholism are based on the personal tolerance to alcohol and various other factors. The same amount of alcohol consumed or same BAC (blood alcohol concentration) in two individuals give different clinical manifestation; one may be under influence and other may not be under influence of alcohol. Chemical analysis of the blood in this examination reveals only the amount or concentration of alcohol.

155

Alcoholic anonymous: It is an association (without having a formed body and place) of people who have given up alcohol. The addicts, who desire to give up alcohol, narrate their bad experiences to other alcoholics through meetings, symposiums, letters, press, etc. Alcoholic intoxication: It is a state occurring in a person due to consumption of alcohol in a quantity sufficient to loose control of his faculty to such an extent that he is unable to perform his activities. Drunkenness: It is a condition which results from excessive intake of alcohol and the person concerned is so much under its influence that: 1. He loses control over his mental faculties. 2. He is unable to perform his duties in which he is engaged at a particular time. 3. He may be a source of danger to himself or others. Features at Different States of Alcohol Consumption Slight: Flushed face, dilated pupils, euphoric, loss of restraints. Under the influence: Flushed face, dilated and sluggish pupils, loss of restraints, increase in reaction time, stagger in sudden turning. Drunk: In addition to the above symptoms, there is staggering gait with reeling and lurching while making sudden turn. Bombay Prohibition Act It is the Act (operated in Maharashtra/Gujarat) in relation to drinking, drunkenness, pleas in relation to drinking of nonprohibited preparation and possession of intoxicant. Some important sections of BP Act are as follows: Sec. 65 and 66(1): Provide penalty for illegal import, export, manufacture, sale, and purchase of an intoxicant without proper license, permit or authorization.

Sec. 62(2): If blood alcohol concentration is not less than 0.05% (50 mg%), then accused person is supposed to prove the cause.

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Sec. 84: Provides penalty for being found drunk or drinking in a common drinking place/house or being present for the purpose of drinking. Punishment of `500. Sec. 85: Provides punishment for being drunk and disorderly in any public place, street, thoroughfare. Punishment for imprisonment of 1–3 months with or without fine of `500. Sec. 129(A): A prohibition officer who has reasonable ground for believing that the person has consumed an intoxicant, is authorised to get such a person medically examined and his blood test for quantitative estimation of alcohol. Rule 3 of BP Act: Deals with clinical examination and certification of a person by RMP in alleged consumption case. Rule 4: Provides for the manner of collection of blood and forwarding to CA. Rule 5: Deals with certificate of test in relation to blood sample examined by the chemical examiner. Rule 117: Prohibition officer authorized to search any person, article or premises believed to provide evidence of possession of intoxication.

Rule 121(1): Opens any package and examines any goods and stop and search any vehicle. Rule 123(1): Seize and detain any articles likely to contain intoxicant. Rule 123(2): Forward the article to nearest police station for CA. Section 117 of Motor Vehicle Act: Offence to drive/attempt to drive a motor vehicle with any quarter of alcohol in blood. In India, the statutory limit of alcohol in blood is 30 mg% u/s 185b of MVA, 19888. The punishment for 1st offence is up to `2000/– or 6 months imprisonment; and for subsequent offence is `3000/- or 2 years imprisonment or both. Table 12.2: BAC in relation to different stages of alcohols intoxication BAC

Different stages

0.05% (0.05 g/dL) 0.10% 0.2% (0.2 g/dL) 0.3% (0.3 g/dL) 0.4% 0.5% 0.6% (0.6 g/dL)

Changes in special test Stimulation Incoordination Confusion Stupor Coma Death

If the BAC is 0.1% and above, then person is usually considered to be under the influence.

FORMALDEHYDE

KEROSENE

NAPHTHALENE (MOTH BALLS)

40% formaldehyde is formalin. It is colorless, pungent irritating odor

It is a clear liquid formed from hydrocarbons obtained from the fractional distillation of petroleum between 150 and 275°C

Properties: White scaly powder which volatiles at room temperature9

Uses 1. Preservation of tissue for histopathology 2. Embalming fluid

Uses 1. Used as fuels/and solvent in paints, pesticides 2. For preserving yellow phosphorus

Uses 1. Moth repellent—as mothballs 2. Deodorant cakes

Action Locally—GIT irritation, and precipitation of protein After absorption it causes systemic acidosis3

Action Locally—irritation of GIT Systemic—nephrotoxic, neurotoxic, respiratory depression

Action The metabolites alpha and beta naphthol and naphthaquinone are powerful hemolytic agents,4 especially in individual with G6PD deficiency9

Inebriant Poison: Alcohols

157

Absorption, fate, and excretion Absorption through mucosa of GIT/RT After absorption it is changed to formic acid (like in methyl alcohol)3

Absorption, fate, and excretion Kerosene is poorly absorbed from GIT but there is often aspiration into respiratory tract especially, if child vomits

Absorption, fate, and excretion Absorbed through mucosa of GIT. It is metabolized in liver and distributed to visceral organs and excreted in urine

Fatal dose: 30–90 ml Fatal period: Within 24 hrs

Fatal dose: 30 ml Fatal period: Not fixed

Fatal dose:8 2–5 gm Fatal period: Uncertain

Clinical features • Nausea, vomiting, diarrhea, abdominal pain confusion, • After absorption it produces systemic acidosis and other features similar to methyl alcohol poisoning.3 • When vapor is inhaled—it causes bronchitis, pneumonitis.3

Clinical features • Vomiting, diarrhea, abdominal pain, smell of

Clinical features • General—nausea, vomiting, abdominal pain, fever,

kerosene in breath convulsion • Headache, giddiness, • Hemolytic manifestation—pallor, drowsiness, confusion, weakness, jaundice, cyanosis, and convulsion, coma dark urine (hemoglobinuria) with • Cough, cyanosis, labored increase WBC count, fragmented breathing, with respiratory RBC, anisopoikilocytosis, Heinz failure, pneumonitis, pulmonary bodies9 edema due to aspiration • Chronic exposure leads to aplastic • Fever10 anemia, hepatic neurosis and jaundice8 • Glycosuria, proteinuria10 • The features of kerosene intoxication are due to aspiration after swallowing.11

Treatment Treatment 1. Stomach wash: 0.1% ammonia 1. Stomach wash: Sodium solution and sodium bicarbonate. Although relatibicarbonate solution3 vely CI, if done with good 2. Demulcent care to avoid aspiration, 3. Antidote: Sodium bicarbonate it is beneficial.10 IV infusion3 2. Artificial respiration and O2 inhalation 3. Liquid paraffin—250 mg oral 4. Symptomatic: Steroids, pantoprazole, IV fluids, antibiotics

Treatment 1. Stomach wash and emesis 2. Avoid demulcent 3. Treat hemolysis with blood transfusion, packed/red cell transfusion or exchange transfusion9

PM findings Stomach: Mucosa—inflamed; Wall—hard and leathery; Content—formalin smell present Adjacent organs: Also becomes hard and inflamed due to the transudation of formalin through stomach Lungs/brain: Congested, edematous Liver/kidneys: Shows fatty degeneration

PM findings On opening the body cavities— smell of kerosene present. Stomach: Mucosa—inflamed; Wall—soft; Content—kerosene smell present Organs: Congested Kidneys: Degenerative changes Lungs: Congested, edematous, pneumonitis

PM findings Not specific Stomach: Mucosa—inflamed; Wall—soft; Content—naphthalene particle with peculiar smell present Organs: Congested Kidneys: Hemorrhagic on cut section Lungs: Congested, edematous

ML aspects 1. Suicidal: Rarely 2. Homicidal: Not occur 3. Accidental: Mostly

ML aspects 1. Suicidal: Rarely 2. Homicidal: Not occur 3. Accidental: Mostly in children

ML aspects 1. Suicidal: Rarely 2. Homicidal: Not occur 3. Accidental: Mostly in children

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Fig. 12.17: Formaldehyde

Fig. 12.18: Kerosene

Fig. 12.19: Naphthalene balls

Fig. 12.20: Stomach in formalin poisoning Table 12.3: Types and examples of different hydrocarbons8 Types

Examples

Aliphatic hydrocarbons

Gasoline, naphtha, mineral spirits, kerosene, turpentine

Halogenated (chlorinated) HC

Organochlorines, CCl4, TCE (trichloroethylene)

Aromatic hydrocarbons

Benzene, toluene, xylene

Inebriant Poison: Alcohols

IMPORTANT QUESTIONS

1. Explain the term ‘spirit’ and ‘liquor’ with examples. Describe metabolism, clinical features and management of ethyl alcohol intoxication. 2. Write different types of beverages with examples. Describe metabolism, clinical manifestation, treatment and medicolegal aspect of methyl alcohol intoxication. 3. What is rectified and denatured spirit? Add a note on Breathalyzer and Widmark formula. Write different hazards and medicolegal aspect of alcohol. 4. What is inebriant poison? Describe clinical features, management and medicolegal aspect of formaldehyde or kerosene poisoning. 5. What are distilled and un-distilled products of alcohols? Describe different factors affecting rate of absorption of alcohol. Describe management of ethyl and methyl alcohol intoxication. Add a note on Bombay Prohibition Act. SPECIFIC LEARNING OBJECTIVES After reading this chapter, the reader should be able to:

• Define inebriants and related terms like alcohols, spirit, liquor, beverages, arrack, proof spirit, etc • Name different inebriant poisons • Classify alcoholic beverages with examples • Enumerate the uses of ethyl/methyl alcohol • Recognize the metabolism of alcohol with fatal dose and fatal period • Explain clinical manifestations, treatment, postmortem findings and medicolegal aspect of ethyl/methyl alcohol intoxication • Enumerate different tests for alcohol • Define drunkenness and BP Act and recognize the basics of breathalyzer

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• Examine alcoholic person and to certify the opinion • Explain clinical features, treatment, postmortem findings and medicolegal aspect of isopropyl alcohol/ kerosene poisoning References 1. Tripathi KD. Ethyl and methyl alcohols. In: Essential of Medical Pharmacology. Jaypee Brothers Medical Publishers (P) Ltd: New Delhi, 7th edn, 2014: 388–96. 2. Longo DL, Fauci AS, Kasper DL, Hauser SL, Jameson JL, Loscalzo J. (edi). Alcohol and alcoholism. In: Harrison’s Principles of Internal Medicine. McGraw-Hill Companies: New York. 18th edn. (vol 2), 2012: 3546–52. 3. Nandy A. Principles of Forensic Medicine. New Central Book Agency (P) Ltd: Calcutta, 2nd edn Reprint, 2004: 517–43. 4. Dikshit PC. Textbook of Forensic Medicine and Toxicology. 2nd edn, PEEPEE Publisher and Distributors (P) Ltd. New Delhi. 2014: 536–47. 5. Slaughter RJ, Mason RW, Beasley DM, Vale JA, Schep LJ. “Isopropanol poisoning”. Clinical Toxicology. 2014; 52 (5): 470–8. doi:10.3109/ 15563650.2014.914527. PMID 24815348. 6. Kruse JA, Methanol poisoning. Intensive Care Med. 1992; 18: 391. https://doi.org/10.1007/ BF01694340. 7. Nand L, Chander S, Kashyap R, Gupta D, Jhobta A. Methyl alcohol poisoning: a manifestation of typical toxicity and outcome. J Assoc Physicians India. 2014 Aug;62(8):756–9. 8. Reddy KSN, Murthy OP. The Essential of Forensic Medicine and Toxicology. 32nd edn, Om Sai Graphics: Hyderabad. 2013: 537–53. 9. Pillay VV. Textbook of Forensic Medicine and Toxicology. Paras Medical Publisher: Hyderabad, 17th edn, 2016: 581–601. 10. Nouri L, Al-Rahim K. Kerosene poisoning in children. Postgraduate Med J. 1970; 46: 71–5. 11. Maheswari A, Gulati S. Kerosene poisoning. Indian Journal of Medical Specialities. 2018; 9(3): 163–6. https://doi.org/10.1016/j.injms. 2018.06. 009

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13 Deliriant Poisons: Datura, Cannabis and Cocaine Deliriants are the substance, which causes delirium, means great excitement and ecstasy. Delirium is an acutely disordered state of mind characterized by altered consciousness, agitation, confusion, delusion, hallucination1 with incoherent speech, and frenzied excitement, occurring in intoxication, fever, metabolic states, etc. Important examples are Datura, cannabis, and cocaine. However, cocaine is potent CNS stimulant, but is described in this chapter.

DATURA

Common Name Thorn apple, Jimson weed, stinkweed. Family: Solanaceae. Plant: Characteristics Datura stramonium—grows in Himalayan altitudes. Datura fustuosa—grows on plains all over India. There are two varieties of Datura fustuosa— niger (with purple flowers), and alba (with white flowers) (Figs 13.1 and 13.2).

ew N

Toxic part: All parts of the plant are poisonous but maximum concentration is in the seeds present in the fruit commonly called ‘Thorn Apple’, which is spherical in shaped having multiple spikes on the surface and containing about 400–500 seeds. The white or purple color flowers are tubular in shape. Datura seeds: Odorless, bitter taste, yellowish brown, larger and thicker than chilli, kidney-shaped, rough surface, have two ridges on their convex surface, on dissection embryos are curved outward near hilum (Fig. 13.3). Datura seeds are similar to chilli (Capsicum) seeds. Points of differences are shown in Table 13.1.

re u g Fi

Fig. 13.1: Datura fustuosa—Alba variety

Fig. 13.2: Datura fustuosa—Niger variety 160

Deliriant Poisons: Datura, Cannabis and Cocaine Table 13.1: Difference between seeds of Datura and Capsicum (chilli) Points

Datura

Chilli

1. Odor 2. Taste

Odorless Bitter

3. Color

Yellowish brown Larger Thick Kidney Rough Two ridges

Pungent Burning Irritating Pale yellow

4. 5. 6. 7. 8.

Size Thickness Shape Surface Ridge on convex surface 9. On cut section2

Embryo curved outward

Smaller Thin Round Smooth No ridge

Embryo curved inward

Capsicum seeds: Pungent irritating smell, burning irritating taste, pale yellow, smaller and thinner, roundish, smooth surface, no double ridges on the margins, on dissection embryos are curved inward near hilum (Fig. 13.4). Active Principles (Belladonna alkaloids)1 • Hyoscine (scopolamine) • Hyoscyamine • Atropine.

Fig. 13.3: Datura seeds

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Uses

1. Atropine as one of the active principles is used as medicine in:3 a. Antidote for organophosphates and carbamates poisoning and mushroom poisoning. b. Anti-secretory in pre-anesthetic medication. c. Mydriatic. d. Antispasmodic. e. Bronchial asthma. 2. Datura seeds powder is used as kicking agent in the alcohol. 3. The seeds are also used in preparing sui (needle) from Abrus precatorius seeds. Fatal Dose Atropine—50–60 mg, hyoscine—10 mg. Seeds—75–100 seeds, for stupefying uses— 40–50 seeds. Fatal Period 24 hours.

Absorption, Metabolism, and Excretion • It is absorbed through mucosa of GIT/RT. • Metabolized in liver (atropine is destroyed by enzyme atropinase). • Excreted through urine.

Fig. 13.4: Capsicum seeds

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• Atropine is retained for long periods in dead bodies. Action • It blocks the ACh receptor and thus produces sympathomimetic or parasympatholytic action. • CNS—it first stimulates and then depresses. Clinical Manifestation The alkaloids of datura stimulate the higher centers of the brain and then the motor centers. Thus, they inhibit secretion, dilate the cutaneous blood vessels, dilate the pupils and stimulate the heat regulating center. The initial stimulation (stage of delirium) is followed by depression and paralysis of the vital centers in the medulla (stage of coma). Central effects of alkaloids are usually psychotic-like symptoms with photophobia, blurred vision, seizure and even coma, 4,5 whereas it causes peripheral symptoms like mydriasis, dry mouth, flushing, tachycardia, fever and urinary retention.4,5 The symptoms are classically described as classic phrase—dry as a bone, red as a beet, blind as a bat, hot as a hare, and mad as a wet hen. • There is bitter taste in mouth, difficulty in speech/deglutition, vomiting, abdominal pain. Body temperature is raised and skin is dry and hot due to inhibition of sweat secretion and stimulation of heat regulating centers (hot as a hare). Face is flushed due to dilatation of cutaneous blood vessels (red as a beet). Conjunctiva congested, pupils are dilated, insensitivity to light, blurring/ double vision (blind as a bat). Pulse is rapid, respiration is hurried. This is followed by giddiness, staggering gait, incoordination of muscle. • The mind is affected, first restless and confused, later becomes delirious, talkative and mutters indistinct words (mad as a hen). • This is followed by mania, convulsion, delirium and hallucination (visual/ auditory). The person tries to run away from the place, grasp imaginary object, and put

imaginary threads in the imaginary needles with fingers.6 • This excitation phase is followed by depressive phase, where the person is in deep sleep/coma, respiratory depression and death. Thus, the main features can better be summarized under 9 Ds 1 mistaken for drunkenness and anticholinergic poisoning: 1. Dryness of mouth/throat, nausea, vomiting. 2. Difficulty in talking. 3. Dysphagia. 4. Dilated pupils, diplopia. 5. Dry, hot skin. 6. Drunken gait (ataxia). 7. Delirium, with disorientation, confusion, agitation, and hallucinations. 8. Drowsiness leading to coma. 9. Dysuria (urinary retention). Death is due to respiratory failure or cardiac arrhythmias. Treatment 1. Stomach wash with KMnO4 or Tannic acid 2. Purgatives 3. Antidotes: a. Physostigmine7 0.5–2 mg IV, 1–2 hrly, relieve both cerebral and peripheral symptoms (usually preferred). OR b. Neostigmine (2.5 mg IV every 3 hourly), or pilocarpine nitrate (6–15 mg SC) relieves only peripheral symptoms. OR 4. Symptomatic: a. Inj chlorpromazine (50–100 mg) or inj diazepam, if patient is violent. b. Cold sponging. Postmortem Findings • • • • •

Not specific. Signs of asphyxia. Stomach: Broken seeds of datura. Visceral organs are congested. Datura resists putrefaction and found even in decomposed bodies.

Deliriant Poisons: Datura, Cannabis and Cocaine

Medicolegal Aspect 1. Accidental: While using for other purposes, mistaken with capsicum seeds usually by children, adulterated country liquor/ toddy (mixed with datura seeds powder, chloral hydrate for kicking effect). 2. Suicidal: Mostly reported from rural areas. 3. Homicidal: Extremely rare. 4. Stupefying agents: Prior to robbery, kidnapping or rape , the seeds are crushed and mixed with food, tea, drink, paan, prasad and given to unwary travellers by co-passengers to produce confusion, disorientation, and loss of consciousness. Children may be easily kidnapped by giving them candy or sweet mixed with datura. They follow all the instructions of the person (who gave these sweet) to follow him. Likewise, women have been abducted, robbed or raped.

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5. Aphrodisiac agent: To increase sexual desire. 6. Datura abuse due to its hypnotic and hallucinogenic properties.1 Chemical Test: Mydriatic Test2 If a drop of stomach content (having Datura) is poured in rabbit’s eye, then there is dilatation of pupil. Laboratory Investigation Raised liver enzymes like LDH, CPK, etc. without myoglobinuria and normal kidney function test.8

Fig. 13.6: Datura fustuosa—alba variety

Fig. 13.5: Datura fustuosa—niger variety (Courtesy: Dr. Manish Shrigiriwar)

Fig. 13.7: Datura fustuosa—niger variety with purple flower

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Fig. 13.8a: Thorn apple—Datura fruit (alba)

Fig. 13.8b: Thorn apple—Datura fruit (niger)

Fig. 13.9: Datura fustuosa—purple flower

CANNABIS

COCAINE (Erythroxylum Coca)

Common name: Indian hemp

Common names: Coke, snow, cadillac, white lady, etc.

Family: Cannabaceae

Family1: Erythroxylaceae

Cannabis sativa is having two varieties: Cannabis indica—grows all over India. Cannabis mexicana—grows in Mexico. The term cannabis refers to the flowering and fruiting tops of Cannabis plant. Cannabis is a tall weed growing up to 15 feet in height and it is a dioecious plant, i.e. the sexes are separated. All part of the plant is toxic. But its cultivation and marketing is under strict legislation and control under government. It is a drug of dependence and consumed in different preparations containing different concentrations of active principle, namely Tetrahydrocannabinol (THC).

Cocaine is an alkaloid, extracted from the leaves of the coca tree, namely Erythroxylum coca and E. novogranatense. They grow in mountains of South America, Indonesia, and India. The plant grows to a height of 7–10 feet. The green leaves have two longitudinal curved lines on either side of the thick midrib, clearly seen on the undersurface. The yellowish-white flowers are small in clusters on short stalk, which mature into red berries. Cocaine is the strongest drug of psychological dependence but also causes strong physical dependence that makes it a notorious drug of addiction.

Deliriant Poisons: Datura, Cannabis and Cocaine

Fig. 13.10: Cannabis plant

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Fig. 13.11: Erythroxylum coca (cocaine plant)

Cannabis is usually abused among sadhussanyasis, college students and western musicians/ painters, however, physical dependence is not common.1

Cocaine is usually abused by the upper classes of society to enhance self-image or improve professional performance1

Common preparations/forms of cannabis2,9 and concentration of THC in brackets 1. Bhang: (Siddi/patti) prepared from dried leaves and stem (2–5% THC), and consumed orally. 2. Majun: Sweet preparation of bhang after treating with sugar, flour, milk 3. Ganja: Prepared from flowering tops of female plant (5–10%). It is rusty brown and is smoked 4. Charas/hashish: It is resinous extract from flowering tops and leaves. It is dark green or brown-colored powder2 (25–40%) is usually smoked along with tobacco.

Cocaine is available in various forms:2 1. Cocaine hydrochloride: It is white, shiny crystalline odorless substance with a bitter, numbing taste. Typically used for injection/ snorting, but can also be ingested. 2. Cocaine sulphate (Cocoa paste): It is a crude product contaminated with solvents, used for smoking. 3. Crack: It is prepared by heating cocaine with baking soda and water. It is used for smoking, gives off cracking sound, hence named. 4. Speedball: Cocaine is taken with heroine by IV route for higher euphoria.

Ganja is smoked either as it is or mixed with tobacco in a pipe/hookah/chilam or in the form of cigarette. The cigarette preparation of ganja is called ‘Reefer’.2 When ganja is smoked in a pipe, then it is called Marijuana.1 Bhang is mixed with fruit juice or milk and consumed during Holi and Navaratri in North India.1 There is a characteristic odor like that of a burnt rope in all cannabis preparations when smoked. Uses:9 At present, cannabis is a banned drug in India and most parts of the world. Cannabis has been the most popular recreational and ritualistic intoxicant used for millennia 1. Antiemetic against vomiting induced by anticancer drugs 2. Treatment of convulsions/anxiety1 and migraine 3. As bronchodilator in asthma. 4. To reduce IOT in glaucoma.

Uses: 1. Medicinally used as local anesthetic agent in minor surgery/procedures 2. Brompton’s cocktail: It contains cocaine, morphine, chlorpromazine, and alcohol. It was previously popular as a pain reliever in terminal cancer1 3. Used as a snuff to reduce appetite and feeling of fatigue10 4. Used as aphrodisiac and as a pleasant intoxicant10

Fatal dose:2 Very high, fatality is uncommon Charas—2 gm; Ganja—8 gm Bhang—10 gm/kg body weight Fatal period: 12 hours to a few days

Fatal dose Oral—1.5 gm Injection—1 gm (hypodermic injection 40 mg) Fatal period: A few min to 2 hours

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Cannabis

Cocaine

Absorption, fate, and excretion Absorbed through mucosa of GIT and also through RT when smoked Metabolized in liver Excreted through urine, feces, bile

Absorption, fate, and excretion Absorbed through mucosa of GIT/RT/nose (when used as snuff) Metabolized in liver Excreted through urine

Action 1. It is a hallucinogen causes excitement followed by sleep 2. CNS—stimulant

Action 1. It is a strong amino-oxidase inhibitor and potentiates the effects of adrenaline or noradrenaline 2. CNS—stimulant and local anesthetic11

Fig. 13.12: Ganja

Fig. 13.15: Bhang

Fig. 13.13: Chilam

Fig. 13.16: Majun

Clinical features Acute cannabis poisoning: Generally considered, cannabis is not very toxic and fatal. It is a hallucinogen. In acute poisoning, it causes excitement followed by sleep. The manifestations depend on individual tolerance and routes of administration and are grouped into two stages. a. Stage of excitement/euphoria and release of inhibition • Sense of well-being, excitement, euphoria, talkativeness, uncontrollable laugh, marked

Fig. 13.14: Cocaine powder

Fig. 13.17: Charas

Clinical features Acute cocaine poisoning Cocaine toxicity produces a hyper-adrenergic state characterised by hypertension, tachycardia, tonicclonic seizures, dyspnea, and ventricular arrhythmias.12 It is a powerful CNS stimulant causing in sequence euphoria—excitement—confusion—restlessness— tremor and twitching of muscle—convulsion— unconsciousness—respiratory depression—death, in a dose dependant manner.11 It also stimulates vagal centre—bradycardia; vasomotor centre—rise in BP;

Deliriant Poisons: Datura, Cannabis and Cocaine

167

increase in appetite specially sweet, craving for sleep, purposeless muscular movement and visual hallucination and ideas (sees nude beautiful women dancing before him, playing music, and singing romantic songs) • Motor incoordination, tachycardia, conjunctival congestion, miosis • There may be disorientation of time, place and person and gradually patient passes to next stage b. Stage of narcosis • It is characterized by giddiness, confusion and ataxia. The person is in dreamy state, with frightful hallucination and delirium. Sometimes there is development of homicidal tendency or thanatophobia • There is tingling and numbness of skin or generalized anesthesia and becomes deeply narcotized • Intravenous use can cause headache, vertigo, dyspnea, diplopia, hypotension, and renal failure1 • Usually recovery occurs after a deep sleep. • Death is due to respiratory failure

Vomiting centre—nausea, vomiting; temperature regulating centre—pyrexia (fever).11 The manifestations are grouped in two stages. a. Stage of stimulation: • Initially there is a sense of well-being, euphoria with excitement, confusion, restlessness, increases reflexes with increase in the BP, heart rate, and respiratory rate, and ventricular arrhythmia. • There may be sudden rise of temperature with rigor (cocaine fever), dryness of mouth, dysphagia, tingling and numbness of tongue/ mouth. • Pupils—dilated • There may be hallucination, muscle twitching, tremor, and convulsion and gradually passed to next stage. b. Stage of depression: • There may be paralysis of muscle, loss of reflexes, collapse, coma and death. • Cocaine washed out syndrome1: Sometimes, there may be lethargy and decreased level of consciousness persisting up to 24 hours followed by recovery.

Chronic cannabis poisoning: Seen in person who consumed for long period with the development of strong psychological dependence • There is general loss of weight/appetite, weakness, emaciation, tremor, impotence • There is mental and moral deterioration/ degradation, insanity and sometimes person turns violent and may ‘run amok’, who go on killing person who comes in his way to either surrender or killing himself ultimately. The person suffers from some hallucination or delusion of persecution/infidelity, due to which the patient is overpowered by an irresistible impulse to destroy life and property • Amotivational syndrome:1,9 Chronic young abusers gradually become lethargic, apathetic with lack of interest and concentration in work • Toxic psychosis: Decreased concentration, memory and learning abilities2 • Hashish insanity:1 Heavy abuse causes paranoid psychosis with violent behavior, culminating in homicide or suicide (run amok) • Increased susceptibility to pharyngitis, bronchitis, asthma, and gynecomastia (in males)

Chronic cocaine poisoning: Cocainism/cocainomania— Immediately upon intake, there is euphoria (rush), for an hour or more followed by rebound depression (crash). To get rid of the unpleasant effects of the later, the individual feels compelled to take the drug again, and the vicious cycle continues until physical, financial, or drug resources are exhausted. • There is loss of weight/ appetite, weakness, tremors, impotence, insomnia, and emaciation • There is mental and moral degradation. There is degeneration of CNS with development of dementia and may get involved in crimes • Psychosis:1 There is tactile hallucination with feeling of insects crawling on the skin, or of sand lying under the skin (cocaine bugs, Magnan’s syndrome). The person may suffer from dreadful hallucination and delusion of persecution and melancholia • Sexual perversion in males and erotic tension/ nymphomania in females are characteristic feature of chronic cocaine takers • There is blackish pigmentation of tongue and teeth, perhaps due to the action of saliva and lime on cocaine when taken orally, and ulceration/ perforation of nasal septum when cocaine is sniffed

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Treatment of acute poisoning—cannabis 1. Stomach wash with warm water, in case the drug has been ingested, and purgatives 2. Artificial respiration 3. Antidotes—no specific antidotes 4. Supportive: • Benzodiazepines (0.5 mg/kg IV) for agitation and convulsion12 • Haloperidol or other antipsychotic for psychosis • Maintenance of nutrition and • Strong tea/coffee by oral or per rectum

DEATH occurs due to hazards like: a. Inhalation of vomitus b. Accidents—injury, electrocution, drowning, etc. when the person takes cannabis

Treatment of acute poisoning—cocaine 1. Stomach wash with activated charcoal1 when ingested 2. Antidote: Amyl nitrite inhalation 3. Artificial respiration and O2 inhalation 4. Symptomatic/supportive: • Benzodiazepines (0.5 mg/kg IV over an 8 hours period13) for restlessness and convulsions • Haloperidol or other antipsychotic for psychosis, and • Ice bath for hyperthermia 5. For cardiac irritability:6 a. Vagal stimulant—acetylcholine HCl 1 mg IV or carbachol 0.25 mg IV b. Inhibit cholinesterase enzyme—100 mg procainamide IV c. Slow injection of dilute phenoxybenzamine 10 mg has antiadrenaline action d. Propranolol (0.5–1 mg IV)13 for hypertension and ventricular arrhythmia DEATH due to respiratory failure or cardiac arrest.

Treatment of chronic poisoning:1 1. Gradual withdrawal of the drug 2. Diazepam for anxiety 3. Antipsychotics for psychosis; Psychotherapy

Treatment of chronic poisoning 1. Gradual withdrawal of the drug 2. Psychotherapy

PM findings • Not specific • Suggestive of asphyxia

PM findings Acute poisoning: Nothing specific • Suggestive of asphyxia and cardiac failure • Cerebral and pulmonary edema • Generalized visceral congestion Chronic poisoning:1 • Evidence of nasal erosions, ulceration, or perforation (in “snorters”). Nasal swabs must be taken for chemical analysis

Medicolegal aspects 1. Accidental: Mostly due to over indulgence. Death has been reported in young adult male (who had undergone open heart surgery) after consuming bhang during Hindu festival14 2. Suicidal: Rare 3. Homicidal: Rare 4. Stupefying: Used prior to robbery, kidnapping or rape 5. The person committing a crime under this condition will not be held responsible for the Act under Section 84 of IPC 6. Abrupt stoppage after habitual use can result in a mild withdrawal reaction characterized by restlessness, insomnia, anorexia, and nausea

Medicolegal aspects 1. Suicidal: Not used 2. Homicidal: Not popular 3. Accidental: Due to overdose from its intradermal/ urethral or other uses as a drug of abuse/addiction (causes both psychological and physical dependence) 4. Aphrodisiac: Increases the duration of sex performance when used locally by causing desensitization of the glans penis 5. To improve professional performance

Deliriant Poisons: Datura, Cannabis and Cocaine

169

Body packer:15 The smuggler smuggled contraband drugs (mostly cocaine/heroine and amphetamines, hashish and marijuana), across international border in specially devised packages in the carrier’s rectum, vagina or alimentary canal. Typically the drug is wrapped in several layers of latex by using condoms, gloves or even toy balloons. Up to 214 packages have been found in a single “mule” means ‘potli or sack containing packages’. The packages, which are round or oval of 1–2 cm in diameter, usually contain 3–7 gm of narcotics. The smugglers are termed “packer”, “swallowers” or “stuffers”. All these packages are removed from GIT by taking cathartics or rectal suppositories or disposable enemas. Sometimes the packing may burst, leading to overdose, collapse and acute poisoning (c/s body packers syndrome/ Minipacker syndrome). Diagnosis of an asymptomatic body packer: It can be diagnosed by abdominal X-ray or ultrasound/ CT scan (if X-ray is unclear).15 Water-soluble iodinated contrast material has been given orally to confirm or exclude body packages. Treatment of body packer syndrome:1 1. Asymptomatic patients: a. Whole bowel irrigation with polythylene glycol solution. However, it can dissolve the heroin from a package, rupturing it and increasing absorption of heroin. b. Hence, low volume phosphosoda enemas or high volume saline enemas are given when all packages pass into the colon from the stomach. c. Metoclopramide 10 mg, 8 hourly, may be administered to encourage gastric emptying. d. It may be advisable to empty the rectum first by a bisacodyl suppository. 2. Symptomatic patients: It must be managed with specific drugs, activated charcoal, and whole bowel irrigation. Intestinal perforation or obstruction by packets requires surgical intervention.

IMPORTANT QUESTIONS

1. Enumerate deliriant poisons. Describe clinical manifestation, treatment, postmortem features and medicolegal aspect of Datura poisoning. 2. Write differences between Datura seeds and capsicum seeds. Describe clinical features and treatment of Datura poisoning. Add a note on uses of Datura. 3. Write different preparations of Cannabis. Describe clinical features, treatment and medicolegal aspects of Cannabis poisoning. 4. Describe clinical features and treatment of cocaine poisoning. Add a note on body packer syndrome. SPECIFIC LEARNING OBJECTIVES

After reading this chapter, the reader should be able to: • Name the different deliriant poisons • Differentiate Datura and Capsicum seeds • Enumerate active principles, uses and fatal dose/period of Datura

• Explain clinical manifestations, treatment, postmortem findings and medicolegal aspects of Datura intoxication • Enumerate 9 Ds of Datura poisoning • Enlist active principle, uses and different preparations of Cannabis • Define run amok and explain clinical manifestations of acute and chronic Cannabis poisoning • Explain the management and medicolegal aspect of Cannabis poisoning • Enlist various uses and different forms of cocaine • Define cocaine fever/Magnan’s syndrome and explain clinical manifestations of acute and chronic cocaine poisoning • Explain the treatment and medicolegal aspect of cocaine poisoning • Understand the significance of body packer syndrome with its diagnosis and treatment References 1. Pillay VV. Textbook of Forensic Medicine and Toxicology. 17th edn, Paras Medical Publisher: Hyderabad. 2016: 618–33.

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2. Dikshit PC. Textbook of Forensic Medicine and Toxicology. 2nd edn, PEEPEE Publisher and Distributors (P) Ltd. New Delhi. 2014: 528–35. 3. Tripathi KD. Anticholinergic drugs and drugs acting on autonomic ganglia. In: Essential of Medical Pharmacology. 7th edn, Jaypee Brothers Medical Publishers (P) Ltd: New Delhi. 2014: 113–23. 4. Krenzelok EP. Aspects of Datura poisoning and treatment. Clinical Toxicology 2010;48(2):104–10. 5. Forrester MB. Jimsonweed (Datura stramonium) Exposures in Texas, 1998–2004. Journal of Toxicology and Environmental Health. 2006;69 (19):1757–62. 6. Nandy A. Principles of Forensic Medicine. 2nd edn, Reprint. New Central Book Agency (P) Ltd: Calcutta. 2004: 517–43. 7. Tripathi KD. Cholinergic system and drugs. In: Essential of Medical Pharmacology. 7th edn, Jaypee Brothers Medical Publishers (P) Ltd: New Delhi. 2014: 99–112. 8. Mohammad Arefi, Nasrin Barzegari, Mahboubeh Asgari, Siamak Soltani, Naeimeh Farhidnia, Fardin Fallah. Datura poisoning, clinical and laboratory findings. Report of five cases. Rom J Leg Med. 2016;24:30–11. DOI: 10.4323/rjlm.

9.

10. 11.

12.

13.

14. 15.

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Cerebral Depressant

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14 Cerebral Depressant Cerebral depressants are the drugs which cause CNS depression. These drugs are sedative (that subduces excitement without sleep) and hypnotic (that induces sleep). It includes barbiturates and benzodiazepines. Bromide, chloral hydrate, and paraldehyde are no longer used as sedative–hypnotic.

BARBITURATES

BENZODIAZEPINES 1,2

It is the derivative of barbituric acid (malonylurea). Barbiturates have been popular hypnotic and sedatives up to 1960s.

Initially BDZs introduce as anti-anxiety drug, but replaced barbiturates as hypnotics and sedatives after 1960s.

Uses: Medicinal uses in:1 1. Psychiatric disorder 2. Epilepsy/seizure disorder (grand mal) 3. For induction and maintenance of general anesthesia (when given IV) 4. IV thiopentone—used as truth serum in narcoanalysis

Uses: Medicinal uses in:1 1. Insomnia 2. Epilepsy/seizure disorder and strychnine poisoning 3. Anxiety disorders 4. As sedatives and hypnotics displacing the barbiturates 5. As muscle relaxant—centrally acting

Classification: According to duration of action a. Long acting barbiturates (6–12 hours): Mephobarbitone, phenobarbitone b. Intermediate acting (3–6 hours): Amobarbitone, aprobarbitone, butobarbitone c. Short acting (